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<!DOCTYPE html><html lang="en"><head><title data-react-helmet="true">The role of adenosinergic pathway in human autoimmune diseases</title> <meta data-react-helmet="true" name="viewport" content="width=device-width, initial-scale=1, maximum-scale=5, viewport-fit=cover"/><meta data-react-helmet="true" property="og:site_name" content="scite.ai"/><meta data-react-helmet="true" property="og:type" content="website"/><meta data-react-helmet="true" property="twitter:card" content="summary_large_image"/><meta data-react-helmet="true" name="twitter:site" content="@scite"/><meta data-react-helmet="true" property="title" content="The role of adenosinergic pathway in human autoimmune diseases"/><meta data-react-helmet="true" property="og:title" content="The role of adenosinergic pathway in human autoimmune diseases"/><meta data-react-helmet="true" property="twitter:title" content="The role of adenosinergic pathway in human autoimmune diseases"/><meta data-react-helmet="true" property="og:image" content="http://image.thum.io/get/ogImage/https://scite.ai/reports/the-role-of-adenosinergic-pathway-MmRgpW?bannerClosed=true&onboardingOff=true&paywallOff=true&v=2"/><meta data-react-helmet="true" property="twitter:image" content="http://image.thum.io/get/ogImage/https://scite.ai/reports/the-role-of-adenosinergic-pathway-MmRgpW?bannerClosed=true&onboardingOff=true&paywallOff=true&v=2"/><meta data-react-helmet="true" name="description" content="Supporting: 2, Mentioning: 25 - Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases."/><meta data-react-helmet="true" property="og:description" content="Supporting: 2, Mentioning: 25 - Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases."/><meta data-react-helmet="true" property="twitter:description" content="Supporting: 2, Mentioning: 25 - Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases."/><meta data-react-helmet="true" property="og:url" content="https://scite.ai/reports/the-role-of-adenosinergic-pathway-MmRgpW"/><meta data-react-helmet="true" name="citation_title" content="The role of adenosinergic pathway in human autoimmune diseases"/><meta data-react-helmet="true" name="citation_doi" content="10.1007/s12026-016-8870-2"/><meta data-react-helmet="true" name="citation_author" content="Dong, Ke"/><meta data-react-helmet="true" name="citation_author" content="Gao, Zhaowei"/><meta data-react-helmet="true" name="citation_author" content="Zhang, Huizhong"/><meta data-react-helmet="true" name="citation_year" content="2016"/><meta data-react-helmet="true" name="citation_journal_title" content="Immunologic Research"/><meta data-react-helmet="true" name="citation_volume" content="64"/><meta data-react-helmet="true" name="citation_issue" content="5-6"/><meta data-react-helmet="true" name="citation_abstract" content="Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases."/><meta data-react-helmet="true" name="citation_public_url" content="https://doi.org/10.1007/s12026-016-8870-2"/> <link data-react-helmet="true" rel="preconnect" href="https://cdn.scite.ai" crossorigin="true"/><link data-react-helmet="true" rel="preconnect" href="https://fonts.googleapis.com"/><link data-react-helmet="true" rel="preconnect" href="https://fonts.gstatic.com" crossorigin="true"/><link data-react-helmet="true" rel="shortcut icon" href="https://cdn.scite.ai/assets/images/favicon.ico"/><link data-react-helmet="true" rel="stylesheet preload prefetch" as="style" href="https://cdn.scite.ai/assets/css/line-awesome-font-awesome.min.css?v=2"/><link data-react-helmet="true" rel="preload" as="style" href="https://fonts.googleapis.com/css2?family=IBM+Plex+Sans:wght@200;300;400;500;600&display=swap"/><link data-react-helmet="true" rel="stylesheet" as="style" href="https://fonts.googleapis.com/css2?family=IBM+Plex+Sans:wght@200;300;400;500;600&display=swap" media="print" onload="this.media='all'"/><link data-react-helmet="true" rel="canonical" href="https://scite.ai/reports/the-role-of-adenosinergic-pathway-MmRgpW"/> <script data-react-helmet="true" src="https://www.recaptcha.net/recaptcha/api.js?render=6LcnMGsqAAAAAJLHdGuust5QwzLk-asKPW5MWbAx"></script><script data-react-helmet="true" type="application/ld+json">{"@context":"http://schema.org","@graph":[{"@id":"#issue","@type":"PublicationIssue","issueNumber":"5-6","datePublished":2016,"isPartOf":{"@id":"#periodical","@type":["PublicationVolume","Periodical"],"name":"Immunologic Research","issn":["0257-277X","1559-0755"],"volumeNumber":"64","publisher":"Springer Science and Business Media LLC"}},{"@type":"ScholarlyArticle","isPartOf":"#issue","description":"Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases.","abstract":"Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases.","sameAs":"https://doi.org/10.1007/s12026-016-8870-2","pagination":"1133-1141","name":"The role of adenosinergic pathway in human autoimmune diseases","headline":"The role of adenosinergic pathway in human autoimmune diseases","author":["Ke Dong","Zhaowei Gao","Huizhong Zhang"],"publisher":{"@type":"Organization","name":"Springer Science and Business Media LLC"},"datePublished":2016}]}</script> <link data-chunk="main" rel="stylesheet" href="https://cdn.scite.ai/assets/dist/main.2a4a881c9257077826c8.css"> <link data-chunk="Report" rel="stylesheet" href="https://cdn.scite.ai/assets/dist/6901.00ffb5a62514ad11206f.css"> <link data-chunk="Report" rel="stylesheet" href="https://cdn.scite.ai/assets/dist/6392.ee3f7fe674ceac954f77.css"> </head> <body><div id="scite-app"><div class="ReportApp__layout___ljMuO"><div><nav class="NavBar__navBarContainer___skQfv"><div 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Link__blueLink___BhE5_" tabindex="0" href="/authors/zhaowei-gao-JWW6A9"><span>Zhaowei Gao</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/air-force-medical-university-jQpV">2</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/huizhong-zhang-K6mRyG"><span>Huizhong Zhang</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/air-force-medical-university-jQpV">3</a></sup></div><span> </span></div></div><div class="TitlePaper__abstractWrapper___S7D_F"><span><h2 class="Header__h2___MuBOH TitlePaper__abstract___GrSZl"><strong>Abstract:</strong>   <span>Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppr…</span><span class="TitlePaper__expandAbstract___O_45M" role="button" tabindex="0">  Show more</span></h2></span></div><a class="TitlePaper__helpMeCta___oNbp1 Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j TitlePaper__helpMeCta___oNbp1" tabindex="0" role="button">Help me understand this report</a></div></div><div class="ReportDropdown__dropdownMenuContainer___G8S6M"><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div><div><div class="ReportPanel__mainLayout___kuDP5"><div class="ReportPanel__filtersLayout___KAxUi"><div class="Filters__filters___FcFPI"><div class="Filters__loadingLayout___i7nI3" style="opacity:0;pointer-events:auto"><div data-testid="circle-spinner" class="CircleSpinner__sciteLoadingRing___nlTrH" style="width:80px;height:80px"><div class="CircleSpinner__ringComponent____iKPi" style="border-color:#0062ff transparent 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d="M4.516 7.548c0.436-0.446 1.043-0.481 1.576 0l3.908 3.747 3.908-3.747c0.533-0.481 1.141-0.446 1.574 0 0.436 0.445 0.408 1.197 0 1.615-0.406 0.418-4.695 4.502-4.695 4.502-0.217 0.223-0.502 0.335-0.787 0.335s-0.57-0.112-0.789-0.335c0 0-4.287-4.084-4.695-4.502s-0.436-1.17 0-1.615z"></path></svg></div></div></div></div><div class="CheckRowCount__sectionRow___vyiE6"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Discussion</span></label><span><span>2</span></span></div><div class="CheckRowCount__sectionRow___vyiE6"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Introduction</span></label><span><span>2</span></span></div><div class="CheckRowCount__sectionRow___vyiE6"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Signaling Pathways and Molecules Modulating Cardiovascular I</span></label><span><span>1</span></span></div></div></div></div><div class="FilterCard__filterCard___bZEVP"><div class="FilterCard__noInput___lsgWM"><div class="FilterCard__filterCardHeader___puB2k" role="button" tabindex="0" aria-label="Expand Citation Types"><div class="FilterCard__tooltip___q395i Tooltip__reference___hgPSY"><p class="FilterCard__header___dRl1u Paragraph__body____m5FY Paragraph__bold___PhFOq">Citation Types </p><i class="FilterCard__icon___iqNMr fa fa-info-circle"></i></div></div><div class=""><div class="Classification__row___s1V6w"><div class="Classification__rowLeft___VoLlX"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Supporting</span></label><div class="Classification__rowType___282g8"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i></div></div><div class="Classification__rowRight___Zxitp"><span class="Classification__count___Y86vw">2</span></div></div><div class="Classification__row___s1V6w"><div class="Classification__rowLeft___VoLlX"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Mentioning</span></label><div class="Classification__rowType___282g8"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i></div></div><div class="Classification__rowRight___Zxitp"><span class="Classification__count___Y86vw">25</span></div></div><div class="Classification__row___s1V6w"><div class="Classification__rowLeft___VoLlX"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Contrasting</span></label><div class="Classification__rowType___282g8"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--contradicting___BpYwd icon-contradicting"></i></div></div><div class="Classification__rowRight___Zxitp"><span class="Classification__count___Y86vw">0</span></div></div><div class="Classification__row___s1V6w"><div class="Classification__rowLeft___VoLlX"><label class="CheckRow__checkRow___Wumpa"><input class="fa fa-lg fa-check Checkbox__checkbox___dGd5x " type="checkbox"/><span class="CheckRow__checkRowLabel___ax_ST">Unclassified</span></label><div class="Classification__rowType___282g8"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--unclassified___Wc9aa icon-unclassified"></i></div></div><div class="Classification__rowRight___Zxitp"><span class="Classification__count___Y86vw">4</span></div></div></div></div></div><div class="FilterCard__filterCard___bZEVP"><div class="FilterCard__noInput___lsgWM"><div class="FilterCard__filterCardHeader___puB2k" role="button" tabindex="0" aria-label="Expand Year Published"><p class="FilterCard__header___dRl1u Paragraph__body____m5FY Paragraph__bold___PhFOq">Year Published </p></div><div class="Filters__yearRange___mtpTm"><div class="CitationsYearBarChart__barChartContainer___fOCtc"><div class="CitationsYearBarChart__barChart___J1Zgl"><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0.75rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:0rem"></div></div></div><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:4.1344949575045735rem"></div></div></div><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:0rem"></div></div></div><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:4.8rem"></div></div></div><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:2.0672474787522868rem"></div></div></div><div class="CitationsYearBarChart__bar___QB0KQ" style="width:16.666666666666668%"><div class="CitationsYearBarChart__barContainer___A2gcx Tooltip__reference___hgPSY"><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__supporting___iMyv8" style="height:0rem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__contradicting___ZRgkC" style="height:NaNrem"></div><div class="CitationsYearBarChart__barPart___aKZ37 CitationsYearBarChart__mentioning___rfif5" style="height:2.0672474787522868rem"></div></div></div></div></div><div><div aria-disabled="false" class="undefined InputRangeFilter__range___i8qUt"><span class="InputRangeFilter__hide___cvWG2 input-range__label--min"><span class="input-range__label-container InputRangeFilter__labelContainer___UOzQG">2017</span></span><div class="InputRangeFilter__track___Fdwrd input-range__track--background"><div style="left:0%;width:100%" class="InputRangeFilter__track___Fdwrd InputRangeFilter__activeTrack___Xb3wK"></div><span class="input-range__slider-container" style="position:absolute;left:0%"><span class="InputRangeFilter__label___uyn35 InputRangeFilter__labelValue___vCEiN InputRangeFilter__labelBottom___LxO3k"><span class="input-range__label-container InputRangeFilter__labelContainer___UOzQG">2017</span></span><div aria-valuemax="2022" aria-valuemin="2017" aria-valuenow="2017" class="InputRangeFilter__slider___CpeJ9" draggable="false" role="slider" tabindex="0"></div></span><span class="input-range__slider-container" style="position:absolute;left:100%"><span class="InputRangeFilter__label___uyn35 InputRangeFilter__labelValue___vCEiN InputRangeFilter__labelBottom___LxO3k"><span class="input-range__label-container 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css-0"></span><style data-emotion="css 1xc3v61-indicatorContainer">.css-1xc3v61-indicatorContainer{display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-transition:color 150ms;transition:color 150ms;color:hsl(0, 0%, 80%);padding:8px;box-sizing:border-box;}.css-1xc3v61-indicatorContainer:hover{color:hsl(0, 0%, 60%);}</style><div class=" css-1xc3v61-indicatorContainer" aria-hidden="true"><style data-emotion="css 8mmkcg">.css-8mmkcg{display:inline-block;fill:currentColor;line-height:1;stroke:currentColor;stroke-width:0;}</style><svg height="20" width="20" viewBox="0 0 20 20" aria-hidden="true" focusable="false" class="css-8mmkcg"><path d="M4.516 7.548c0.436-0.446 1.043-0.481 1.576 0l3.908 3.747 3.908-3.747c0.533-0.481 1.141-0.446 1.574 0 0.436 0.445 0.408 1.197 0 1.615-0.406 0.418-4.695 4.502-4.695 4.502-0.217 0.223-0.502 0.335-0.787 0.335s-0.57-0.112-0.789-0.335c0 0-4.287-4.084-4.695-4.502s-0.436-1.17 0-1.615z"></path></svg></div></div></div></div></div></div><div class="CitationsHeader__settingsButtonLayout___SCS1l"><button class="SettingsButton__btn___P6KmW Button__btn___k1xtO Button__btn--transparent___XnBIC Button__size--medium___yX63r Button__tiny___hya9X" aria-label="Settings button"><i class="SettingsButton__icon___w15lK fa fa-sliders-h"></i><span>Settings</span></button></div></div><div class="PapersList__citationList___nW0RR"><div style="opacity:1;pointer-events:auto"><div class="PaperCard__paperCard___Tkx_L PaperCard__card___rYfBl"><div><div><div class="Citation__citation___I7BGj Citation__citationGrid___yNzom"><div class="Citation__rightCol___rqdSW"><div class="Citation__snippetLayout___VCTXv"><div class="Snippet__snippetWrapper___pL8c1"><span><span><div>“…Thus, down-regulation of CD73 on B cells might tip the balance toward higher AMP concentrations and lower ADO concentrations. It is important to note that different studies have shown that a disturbance in the adenosinergic pathway can lead to an imbalance of pro-and anti-inflammatory effects depending on the local environment and ADO concentration <cite data-doi="10.1016/j.it.2009.04.001">[58,</cite><cite data-doi="10.1016/j.cyto.2017.01.001">[60]</cite><cite class="target" data-doi="10.1007/s12026-016-8870-2">[61]</cite><cite data-doi="10.1111/cei.12354">[62]</cite>; therefore, our data add to the hypothesis that lower concentrations of ADO might be detrimental by causing the increased chronic immune activation observed during chronic HIV infection <cite data-doi="10.1182/blood-2013-02-482406">[2,</cite><cite data-doi="10.1182/blood-2010-11-321646">63]</cite>.…”</div></span></span></div></div><div class="Citation__citeInfo___v24kU"><span class="Citation__section___YjAW3"><b>Section</b>: Discussion</span><span class="Citation__typeInfo___s7iNF"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="Citation__citationType___LuRbr">supporting</span><div class="Tooltip__reference___hgPSY"><div class="Citation__classificationDetails___xRtK5"><span class="Citation__classificationDetail___vPtBx">confidence: 52%</span></div></div></span></div></div><div class="Citation__actions___STMoF"><div class="Tooltip__reference___hgPSY"><i class="CopyButton__copyButton___I1ybw fa fa-copy" role="button" tabindex="0"></i></div><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div aria-hidden="true" class="PaperCard__expandingWrapper___JmHu_" style="overflow:hidden;height:0;opacity:0"><div style="width:fit-content"></div></div></div><div class="PaperCard__grid___NMQAD"><div class="PaperCard__abstractWrapper___Yq394"><div class="Paper__paper___CWi0y"><a class="Paper__title___WkJQP Link__link___plGt2 Link__bold___JGJNO Paper__title___WkJQP" tabindex="0" href="/reports/down-regulation-of-cd73-on-b-4pba0V"><h3 class="Paper__title___WkJQP">Down-regulation of CD73 on B cells of patients with viremic HIV correlates with B cell activation and disease progression</h3></a><div class="Paper__referenceLine___quVTP"><div class="Authors__authors___uWMEz Paper__lineItem___FXrg7"><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/eun-seong-kim-M22vRW"><span>Kim</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">1</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/christin-ackermann-5YEDdA"><span>Ackermann</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">2</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/ilona-toth-ePKQDz"><span>Tóth</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">3</a></sup></div><span> </span></div><span class="Authors__link___k07oy">et al.</span><span> 2017</span></div><span class="Paper__lineItem___FXrg7"><span class="Reference__reference___AIzFu"><span><a class="Link__link___plGt2 Link__underline___K1Y7j" tabindex="0" href="/journals/journal-of-leukocyte-biology-vJlwN"><em>Journal of Leukocyte Biology</em></a></span></span></span></div><div class="Paper__tallyLayout___k19c4"><a class="HorizontalTally__horizontalTally___gMrpx" href="/reports/down-regulation-of-cd73-on-b-4pba0V"><div class="HorizontalTally__inner___AzKR8"><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--publications___MBaqU icon-publications"></i><span class="HorizontalTally__count___ZuxQA">31</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="HorizontalTally__count___ZuxQA">5</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="HorizontalTally__count___ZuxQA">38</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--contradicting___BpYwd icon-contradicting"></i><span class="HorizontalTally__count___ZuxQA">0</span></div></div></div></a></div><div class="Paper__linksLayout___Ql9Qd"><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" href="https://doi.org/10.1189/jlb.5a0816-346r" tabindex="0" role="link" target="_blank" rel="noopener noreferrer nofollow">View full text</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Add to dashboard</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Cite</a></div></div><div aria-hidden="true" style="overflow:hidden;height:0;opacity:0"><div style="width:auto"><p class="Abstract__abstract___V8wNr PaperCard__abstract___lR5RS Paragraph__body____m5FY"><span><span>Recently, alterations of the T cell expression of the ectonucleotidases, CD39 and CD73, during HIV infection have been described. Here, peripheral ( = 70) and lymph nodal B cells ( = 10) of patients with HIV at different stages of disease as well as uninfected individuals were analyzed via multicolor flow cytometry with regard to expression of CD39 and CD73 and differentiation, proliferation, and exhaustion status. Patients with chronic, untreated HIV showed a significantly decreased frequency of CD73-expressing B cells ( < 0.001) compared with healthy controls. Decreased frequencies of CD39CD73 B cells in patients with HIV correlated with low CD4 counts ( < 0.0256) as well as increased proliferation and exhaustion status as determined by Ki-67 and programmed death-1 expression. Down-regulation of CD73 was observed in naive and memory B cells as determined by CD27 and CD21. Neither HIV elite controller patients nor antiretroviral therapy-treated patients had significantly lower CD39 and CD73 expression on B cells compared with healthy controls. Of importance, low CD73 expression on B cells was associated with modulated in vitro B cell function. Further in vivo studies are warranted to evaluate the in vivo role of phenotypic loss of CD73 in B cell dysregulation in HIV.</span></span></p></div></div></div><div class="PaperCard__menu___wXkM0"><a class="PaperCard__textButton___ncs_Z" tabindex="0">show abstract</a><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div class="PapersList__paywalledCites___XIuJQ"><div class="PapersList__paperCardsLayout___dtzN9"><div class="PaperCard__paperCard___Tkx_L PaperCard__card___rYfBl"><div><div><div class="Citation__citation___I7BGj Citation__citationGrid___yNzom"><div class="Citation__rightCol___rqdSW"><div class="Citation__snippetLayout___VCTXv"><div class="Snippet__snippetWrapper___pL8c1"><span><span><div>“…Thus, down-regulation of CD73 on B cells might tip the balance toward higher AMP concentrations and lower ADO concentrations. It is important to note that different studies have shown that a disturbance in the adenosinergic pathway can lead to an imbalance of pro-and anti-inflammatory effects depending on the local environment and ADO concentration <cite data-doi="10.1016/j.it.2009.04.001">[58,</cite><cite data-doi="10.1016/j.cyto.2017.01.001">[60]</cite><cite class="target" data-doi="10.1007/s12026-016-8870-2">[61]</cite><cite data-doi="10.1111/cei.12354">[62]</cite>; therefore, our data add to the hypothesis that lower concentrations of ADO might be detrimental by causing the increased chronic immune activation observed during chronic HIV infection <cite data-doi="10.1182/blood-2013-02-482406">[2,</cite><cite data-doi="10.1182/blood-2010-11-321646">63]</cite>.…”</div></span></span></div></div><div class="Citation__citeInfo___v24kU"><span class="Citation__section___YjAW3"><b>Section</b>: Discussion</span><span class="Citation__typeInfo___s7iNF"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="Citation__citationType___LuRbr">supporting</span><div class="Tooltip__reference___hgPSY"><div class="Citation__classificationDetails___xRtK5"><span class="Citation__classificationDetail___vPtBx">confidence: 52%</span></div></div></span></div></div><div class="Citation__actions___STMoF"><div class="Tooltip__reference___hgPSY"><i class="CopyButton__copyButton___I1ybw fa fa-copy" role="button" tabindex="0"></i></div><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div aria-hidden="true" class="PaperCard__expandingWrapper___JmHu_" style="overflow:hidden;height:0;opacity:0"><div style="width:fit-content"></div></div></div><div class="PaperCard__grid___NMQAD"><div class="PaperCard__abstractWrapper___Yq394"><div class="Paper__paper___CWi0y"><a class="Paper__title___WkJQP Link__link___plGt2 Link__bold___JGJNO Paper__title___WkJQP" tabindex="0" href="/reports/down-regulation-of-cd73-on-b-4pba0V"><h3 class="Paper__title___WkJQP">Down-regulation of CD73 on B cells of patients with viremic HIV correlates with B cell activation and disease progression</h3></a><div class="Paper__referenceLine___quVTP"><div class="Authors__authors___uWMEz Paper__lineItem___FXrg7"><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/eun-seong-kim-M22vRW"><span>Kim</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">1</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/christin-ackermann-5YEDdA"><span>Ackermann</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">2</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/ilona-toth-ePKQDz"><span>Tóth</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-medical-center-hamburg-eppendorf-5GAgV">3</a></sup></div><span> </span></div><span class="Authors__link___k07oy">et al.</span><span> 2017</span></div><span class="Paper__lineItem___FXrg7"><span class="Reference__reference___AIzFu"><span><a class="Link__link___plGt2 Link__underline___K1Y7j" tabindex="0" href="/journals/journal-of-leukocyte-biology-vJlwN"><em>Journal of Leukocyte Biology</em></a></span></span></span></div><div class="Paper__tallyLayout___k19c4"><a class="HorizontalTally__horizontalTally___gMrpx" href="/reports/down-regulation-of-cd73-on-b-4pba0V"><div class="HorizontalTally__inner___AzKR8"><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--publications___MBaqU icon-publications"></i><span class="HorizontalTally__count___ZuxQA">31</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="HorizontalTally__count___ZuxQA">5</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="HorizontalTally__count___ZuxQA">38</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--contradicting___BpYwd icon-contradicting"></i><span class="HorizontalTally__count___ZuxQA">0</span></div></div></div></a></div><div class="Paper__linksLayout___Ql9Qd"><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" href="https://doi.org/10.1189/jlb.5a0816-346r" tabindex="0" role="link" target="_blank" rel="noopener noreferrer nofollow">View full text</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Add to dashboard</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Cite</a></div></div><div aria-hidden="true" style="overflow:hidden;height:0;opacity:0"><div style="width:auto"><p class="Abstract__abstract___V8wNr PaperCard__abstract___lR5RS Paragraph__body____m5FY"><span><span>Recently, alterations of the T cell expression of the ectonucleotidases, CD39 and CD73, during HIV infection have been described. Here, peripheral ( = 70) and lymph nodal B cells ( = 10) of patients with HIV at different stages of disease as well as uninfected individuals were analyzed via multicolor flow cytometry with regard to expression of CD39 and CD73 and differentiation, proliferation, and exhaustion status. Patients with chronic, untreated HIV showed a significantly decreased frequency of CD73-expressing B cells ( < 0.001) compared with healthy controls. Decreased frequencies of CD39CD73 B cells in patients with HIV correlated with low CD4 counts ( < 0.0256) as well as increased proliferation and exhaustion status as determined by Ki-67 and programmed death-1 expression. Down-regulation of CD73 was observed in naive and memory B cells as determined by CD27 and CD21. Neither HIV elite controller patients nor antiretroviral therapy-treated patients had significantly lower CD39 and CD73 expression on B cells compared with healthy controls. Of importance, low CD73 expression on B cells was associated with modulated in vitro B cell function. Further in vivo studies are warranted to evaluate the in vivo role of phenotypic loss of CD73 in B cell dysregulation in HIV.</span></span></p></div></div></div><div class="PaperCard__menu___wXkM0"><a class="PaperCard__textButton___ncs_Z" tabindex="0">show abstract</a><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div class="PaperCard__paperCard___Tkx_L PaperCard__card___rYfBl"><div><div><div class="Citation__citation___I7BGj Citation__citationGrid___yNzom"><div class="Citation__rightCol___rqdSW"><div class="Citation__snippetLayout___VCTXv"><div class="Snippet__snippetWrapper___pL8c1"><span><span><div>“…Deletion of CD39 and CD73 leads to higher levels of anti-RNP antibodies in response to pristane, with CD73 deletion in particular promoting expansion of splenic B cell and T cell populations that likely contribute to autoantibody production. Within the T cell compartment, it is notable that some of these changes (expansion of effector/memory T cells and T H 17 cells) were present independent of pristane administration, which would fit with a general predisposition toward inflammation and autoimmunity conferred by loss of ectonucleotidase activity ( <cite data-doi="10.1016/j.molmed.2013.03.005"> 11 </cite> , <cite data-doi="10.1371/journal.pone.0037100"> 39 </cite> , <cite class="target" data-doi="10.1007/s12026-016-8870-2"> 40 </cite> ). For example, protective roles for ectonucleotidases have been suggested in rheumatoid arthritis ( <cite data-doi="10.4049/jimmunol.1401416"> 41 </cite> , <cite data-doi="10.1073/pnas.1424792112"> 42 </cite> ), juvenile idiopathic arthritis ( <cite data-doi="10.1002/art.38959"> 43 </cite> ), inflammatory bowel disease ( <cite data-doi="10.1073/pnas.0902869106"> 44 </cite> , <cite data-doi="10.1155/2012/260983"> 45 </cite> ), autoimmune hepatitis ( <cite data-doi="10.1002/hep.26583"> 46 </cite> ), and atherosclerosis ( <cite data-doi="10.1093/cvr/cvr218"> 47 </cite> , <cite data-doi="10.1172/jci79514"> 48 </cite> ).…”</div></span></span></div></div><div class="Citation__citeInfo___v24kU"><span class="Citation__section___YjAW3"><b>Section</b>: Discussion</span><span class="Citation__typeInfo___s7iNF"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="Citation__citationType___LuRbr">mentioning</span><div class="Tooltip__reference___hgPSY"><div class="Citation__classificationDetails___xRtK5"><span class="Citation__classificationDetail___vPtBx">confidence: 99%</span></div></div></span></div></div><div class="Citation__actions___STMoF"><div class="Tooltip__reference___hgPSY"><i class="CopyButton__copyButton___I1ybw fa fa-copy" role="button" tabindex="0"></i></div><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div aria-hidden="true" class="PaperCard__expandingWrapper___JmHu_" style="overflow:hidden;height:0;opacity:0"><div style="width:fit-content"></div></div></div><div class="PaperCard__grid___NMQAD"><div class="PaperCard__abstractWrapper___Yq394"><div class="Paper__paper___CWi0y"><a class="Paper__title___WkJQP Link__link___plGt2 Link__bold___JGJNO Paper__title___WkJQP" tabindex="0" href="/reports/ectonucleotidase-mediated-suppression-of-lupus-autoimmunity-RVaZP6G"><h3 class="Paper__title___WkJQP">Ectonucleotidase-Mediated Suppression of Lupus Autoimmunity and Vascular Dysfunction</h3></a><div class="Paper__referenceLine___quVTP"><div class="Authors__authors___uWMEz Paper__lineItem___FXrg7"><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/jason-s-knight-xXeKpg"><span>Knight</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-of-michigan-ann-arbor-WG91">1</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/levi-f-mazza-2N5mrx"><span>Mazza</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-of-michigan-ann-arbor-WG91">2</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/srilakshmi-yalavarthi-ZG4Rpd"><span>Yalavarthi</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/university-of-michigan-ann-arbor-WG91">3</a></sup></div><span> </span></div><span class="Authors__link___k07oy">et al.</span><span> 2018</span></div><span class="Paper__lineItem___FXrg7"><span class="Reference__reference___AIzFu"><span><a class="Link__link___plGt2 Link__underline___K1Y7j" tabindex="0" href="/journals/frontiers-in-immunology-pnD8b"><em>Front. Immunol.</em></a></span></span></span></div><div class="Paper__tallyLayout___k19c4"><a class="HorizontalTally__horizontalTally___gMrpx" href="/reports/ectonucleotidase-mediated-suppression-of-lupus-autoimmunity-RVaZP6G"><div class="HorizontalTally__inner___AzKR8"><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--publications___MBaqU icon-publications"></i><span class="HorizontalTally__count___ZuxQA">24</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="HorizontalTally__count___ZuxQA">3</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="HorizontalTally__count___ZuxQA">16</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--contradicting___BpYwd icon-contradicting"></i><span class="HorizontalTally__count___ZuxQA">0</span></div></div></div></a></div><div class="Paper__linksLayout___Ql9Qd"><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" href="https://doi.org/10.3389/fimmu.2018.01322" tabindex="0" role="link" target="_blank" rel="noopener noreferrer nofollow">View full text</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Add to dashboard</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Cite</a></div></div><div aria-hidden="true" style="overflow:hidden;height:0;opacity:0"><div style="width:auto"><p class="Abstract__abstract___V8wNr PaperCard__abstract___lR5RS Paragraph__body____m5FY"><span><span>ObjectivesCD39 and CD73 are surface enzymes that jut into the extracellular space where they mediate the step-wise phosphohydrolysis of the autocrine and paracrine danger signals ATP and ADP into anti-inflammatory adenosine. Given the role of vascular and immune cells’ “purinergic halo” in maintaining homeostasis, we hypothesized that the ectonucleotidases CD39 and CD73 might play a protective role in lupus.MethodsLupus was modeled by intraperitoneal administration of pristane to three groups of mice: wild-type (WT), CD39−/−, and CD73−/−. After 36 weeks, autoantibodies, endothelial function, kidney disease, splenocyte activation/polarization, and neutrophil activation were characterized.ResultsAs compared with WT mice, CD39−/− mice developed exaggerated splenomegaly in response to pristane, while both groups of ectonucleotidase-deficient mice demonstrated heightened anti-ribonucleoprotein production. The administration of pristane to WT mice triggered only subtle dysfunction of the arterial endothelium; however, both CD39−/− and CD73−/− mice demonstrated striking endothelial dysfunction following induction of lupus, which could be reversed by superoxide dismutase. Activated B cells and plasma cells were expanded in CD73−/− mice, while deficiency of either ectonucleotidase led to expansion of TH17 cells. CD39−/− and CD73−/− mice demonstrated exaggerated neutrophil extracellular trap release, while CD73−/− mice additionally had higher levels of plasma cell-free DNA.ConclusionThese data are the first to link ectonucleotidases with lupus autoimmunity and vascular disease. New therapeutic strategies may harness purinergic nucleotide dissipation or signaling to limit the damage inflicted upon organs and blood vessels by lupus.</span></span></p></div></div></div><div class="PaperCard__menu___wXkM0"><a class="PaperCard__textButton___ncs_Z" tabindex="0">show abstract</a><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div class="PaperCard__paperCard___Tkx_L PaperCard__card___rYfBl"><div><div><div class="Citation__citation___I7BGj Citation__citationGrid___yNzom"><div class="Citation__rightCol___rqdSW"><div class="Citation__snippetLayout___VCTXv"><div class="Snippet__snippetWrapper___pL8c1"><span><span><div>“…Purinergic signaling is highly described in tumoral context ( <cite data-doi="10.1111/imr.12528"> 162 </cite> ) and in autoimmune diseases ( <cite class="target" data-doi="10.1007/s12026-016-8870-2"> 163 </cite> ) but poorly studied in the context of cardiac pathologies. Given the high production rate of ATP and the turnover required to maintain its continuous mechanical work, disruption of heart tissue generates the release of high amounts of ATP to the extracellular space.…”</div></span></span></div></div><div class="Citation__citeInfo___v24kU"><span class="Citation__section___YjAW3"><b>Section</b>: Signaling Pathways and Molecules Modulating Cardiovascular I</span><span class="Citation__typeInfo___s7iNF"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="Citation__citationType___LuRbr">mentioning</span><div class="Tooltip__reference___hgPSY"><div class="Citation__classificationDetails___xRtK5"><span class="Citation__classificationDetail___vPtBx">confidence: 99%</span></div></div></span></div></div><div class="Citation__actions___STMoF"><div class="Tooltip__reference___hgPSY"><i class="CopyButton__copyButton___I1ybw fa fa-copy" role="button" tabindex="0"></i></div><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div><div aria-hidden="true" class="PaperCard__expandingWrapper___JmHu_" style="overflow:hidden;height:0;opacity:0"><div style="width:fit-content"></div></div></div><div class="PaperCard__grid___NMQAD"><div class="PaperCard__abstractWrapper___Yq394"><div class="Paper__paper___CWi0y"><a class="Paper__title___WkJQP Link__link___plGt2 Link__bold___JGJNO Paper__title___WkJQP" tabindex="0" href="/reports/new-insights-into-the-immunobiology-YZ4QGO2"><h3 class="Paper__title___WkJQP">New Insights into the Immunobiology of Mononuclear Phagocytic Cells and Their Relevance to the Pathogenesis of Cardiovascular Diseases</h3></a><div class="Paper__referenceLine___quVTP"><div class="Authors__authors___uWMEz Paper__lineItem___FXrg7"><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/liliana-m-sanmarco-ZGKyAp"><span>Sanmarco</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/universidad-nacional-de-cordoba-yVGl">1</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/natalia-eberhardt-zbx8yb"><span>Eberhardt</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/research-centre-in-biological-chemistry-4Zl8P">2</a></sup></div><span>, </span></div><div class="Authors__author___TTnHS"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/authors/nicolas-ponce-6M4gv9"><span>Ponce</span></a><div class="Tooltip__reference___hgPSY"><sup class="Authors__affiliationSup___Vvflj"><a class="Link__link___plGt2 Link__blueLink___BhE5_" tabindex="0" href="/affiliations/universidad-nacional-de-cordoba-yVGl">3</a></sup></div><span> </span></div><span class="Authors__link___k07oy">et al.</span><span> 2018</span></div><span class="Paper__lineItem___FXrg7"><span class="Reference__reference___AIzFu"><span><a class="Link__link___plGt2 Link__underline___K1Y7j" tabindex="0" href="/journals/frontiers-in-immunology-pnD8b"><em>Front. Immunol.</em></a></span></span></span></div><div class="Paper__tallyLayout___k19c4"><a class="HorizontalTally__horizontalTally___gMrpx" href="/reports/new-insights-into-the-immunobiology-YZ4QGO2"><div class="HorizontalTally__inner___AzKR8"><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--publications___MBaqU icon-publications"></i><span class="HorizontalTally__count___ZuxQA">42</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--supporting___ru3vm icon-supporting"></i><span class="HorizontalTally__count___ZuxQA">0</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--mentioning___zHr8j icon-mentioning"></i><span class="HorizontalTally__count___ZuxQA">26</span></div></div><div class="HorizontalTally__column___d6ltY"><div class="Tooltip__reference___hgPSY"><i class="undefined TypeIcon__typeIcon___USGCh icon TypeIcon__typeIcon--contradicting___BpYwd icon-contradicting"></i><span class="HorizontalTally__count___ZuxQA">0</span></div></div></div></a></div><div class="Paper__linksLayout___Ql9Qd"><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" href="https://doi.org/10.3389/fimmu.2017.01921" tabindex="0" role="link" target="_blank" rel="noopener noreferrer nofollow">View full text</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Add to dashboard</a><a class="Paper__link___YsYPi Link__link___plGt2 Link__blueLink___BhE5_ Link__underline___K1Y7j Paper__link___YsYPi" tabindex="0" role="button">Cite</a></div></div><div aria-hidden="true" style="overflow:hidden;height:0;opacity:0"><div style="width:auto"><p class="Abstract__abstract___V8wNr PaperCard__abstract___lR5RS Paragraph__body____m5FY"><span><span>Macrophages are the primary immune cells that reside within the myocardium, suggesting that these mononuclear phagocytes are essential in the orchestration of cardiac immunity and homeostasis. Independent of the nature of the injury, the heart triggers leukocyte activation and recruitment. However, inflammation is harmful to this vital terminally differentiated organ with extremely poor regenerative capacity. As such, cardiac tissue has evolved particular strategies to increase the stress tolerance and minimize the impact of inflammation. In this sense, growing evidences show that mononuclear phagocytic cells are particularly dynamic during cardiac inflammation or infection and would actively participate in tissue repair and functional recovery. They respond to soluble mediators such as metabolites or cytokines, which play central roles in the timing of the intrinsic cardiac stress response. During myocardial infarction two distinct phases of monocyte influx have been identified. Upon infarction, the heart modulates its chemokine expression profile that sequentially and actively recruits inflammatory monocytes, first, and healing monocytes, later. In the same way, a sudden switch from inflammatory macrophages (with microbicidal effectors) toward anti-inflammatory macrophages occurs within the myocardium very shortly after infection with Trypanosoma cruzi, the causal agent of Chagas cardiomyopathy. While in sterile injury, healing response is necessary to stop tissue damage; during an intracellular infection, the anti-inflammatory milieu in infected hearts would promote microbial persistence. The balance of mononuclear phagocytic cells seems to be also dynamic in atherosclerosis influencing plaque initiation and fate. This review summarizes the participation of mononuclear phagocyte system in cardiovascular diseases, keeping in mind that the immune system evolved to promote the reestablishment of tissue homeostasis following infection/injury, and that the effects of different mediators could modulate the magnitude and quality of the immune response. The knowledge of the effects triggered by diverse mediators would serve to identify new therapeutic targets in different cardiovascular pathologies.</span></span></p></div></div></div><div class="PaperCard__menu___wXkM0"><a class="PaperCard__textButton___ncs_Z" tabindex="0">show abstract</a><div class=""><i class="fa fa-2x fa-ellipsis-h DropdownMenu__dropdownMenuIcon___LGAcI"></i></div></div></div></div></div></div></div><div class="PapersList__loading___Yxc5F" style="opacity:0;pointer-events:none"><div data-testid="circle-spinner" class="CircleSpinner__sciteLoadingRing___nlTrH" style="width:80px;height:80px"><div class="CircleSpinner__ringComponent____iKPi" style="border-color:#0062ff transparent transparent transparent;width:64px;height:64px;margin:8px;border-width:8px"></div><div class="CircleSpinner__ringComponent____iKPi" style="border-color:#0062ff transparent transparent transparent;width:64px;height:64px;margin:8px;border-width:8px"></div><div class="CircleSpinner__ringComponent____iKPi" style="border-color:#0062ff transparent transparent transparent;width:64px;height:64px;margin:8px;border-width:8px"></div><div class="CircleSpinner__ringComponent____iKPi" style="border-color:#0062ff transparent transparent transparent;width:64px;height:64px;margin:8px;border-width:8px"></div></div></div></div></div></div></div></div></div></div></div><div class="Footer__layout___jrAhC"><div class="Footer__mainLayout___MVOfi"><div class="Footer__aboutContainer___TwE0S"><img width="128px" height="41px" alt="scite logo" src="https://cdn.scite.ai/assets/images/logo.svg"/><p class="Paragraph__body____m5FY">scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.</p><div class="Footer__contact___DGc_M"><h6 class="Header__h6___QzBvp">Contact Info</h6><div><p class="Footer__address___VMUTY Paragraph__body____m5FY">customersupport@researchsolutions.com</p><p class="Footer__address___VMUTY Paragraph__body____m5FY">10624 S. 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It is important to note that different studies have shown that a disturbance in the adenosinergic pathway can lead to an imbalance of pro-and anti-inflammatory effects depending on the local environment and ADO concentration \u003Ccite data-doi=\"10.1016\u002Fj.it.2009.04.001\"\u003E[58,\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1016\u002Fj.cyto.2017.01.001\"\u003E[60]\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1007\u002Fs12026-016-8870-2\"\u003E[61]\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1111\u002Fcei.12354\"\u003E[62]\u003C\u002Fcite\u003E; therefore, our data add to the hypothesis that lower concentrations of ADO might be detrimental by causing the increased chronic immune activation observed during chronic HIV infection \u003Ccite data-doi=\"10.1182\u002Fblood-2013-02-482406\"\u003E[2,\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1182\u002Fblood-2010-11-321646\"\u003E63]\u003C\u002Fcite\u003E.","lang":"en","langConfidence":"0.8999999761581421","refLocation":"b57\u002F1","memberId":286,"selfCites":[],"snippetHidden":false},{"id":2153119375,"source":"10.3389\u002Ffimmu.2018.01322","target":"10.1007\u002Fs12026-016-8870-2","negative":0.020929889380931852,"positive":0.05610150471329689,"neutral":1,"section":"discussion","type":"mentioning","typeConfidence":1,"snippet":"Deletion of CD39 and CD73 leads to higher levels of anti-RNP antibodies in response to pristane, with CD73 deletion in particular promoting expansion of splenic B cell and T cell populations that likely contribute to autoantibody production. Within the T cell compartment, it is notable that some of these changes (expansion of effector\u002Fmemory T cells and T H 17 cells) were present independent of pristane administration, which would fit with a general predisposition toward inflammation and autoimmunity conferred by loss of ectonucleotidase activity ( \u003Ccite data-doi=\"10.1016\u002Fj.molmed.2013.03.005\"\u003E 11 \u003C\u002Fcite\u003E , \u003Ccite data-doi=\"10.1371\u002Fjournal.pone.0037100\"\u003E 39 \u003C\u002Fcite\u003E , \u003Ccite data-doi=\"10.1007\u002Fs12026-016-8870-2\"\u003E 40 \u003C\u002Fcite\u003E ). For example, protective roles for ectonucleotidases have been suggested in rheumatoid arthritis ( \u003Ccite data-doi=\"10.4049\u002Fjimmunol.1401416\"\u003E 41 \u003C\u002Fcite\u003E , \u003Ccite data-doi=\"10.1073\u002Fpnas.1424792112\"\u003E 42 \u003C\u002Fcite\u003E ), juvenile idiopathic arthritis ( \u003Ccite data-doi=\"10.1002\u002Fart.38959\"\u003E 43 \u003C\u002Fcite\u003E ), inflammatory bowel disease ( \u003Ccite data-doi=\"10.1073\u002Fpnas.0902869106\"\u003E 44 \u003C\u002Fcite\u003E , \u003Ccite data-doi=\"10.1155\u002F2012\u002F260983\"\u003E 45 \u003C\u002Fcite\u003E ), autoimmune hepatitis ( \u003Ccite data-doi=\"10.1002\u002Fhep.26583\"\u003E 46 \u003C\u002Fcite\u003E ), and atherosclerosis ( \u003Ccite data-doi=\"10.1093\u002Fcvr\u002Fcvr218\"\u003E 47 \u003C\u002Fcite\u003E , \u003Ccite data-doi=\"10.1172\u002Fjci79514\"\u003E 48 \u003C\u002Fcite\u003E ).","lang":"en","langConfidence":"0.8999999761581421","refLocation":"b40\u002F1","memberId":1965,"selfCites":[],"snippetHidden":false},{"id":2142640436,"source":"10.3389\u002Ffimmu.2017.01921","target":"10.1007\u002Fs12026-016-8870-2","negative":0.01478925347328186,"positive":0.0075345030054450035,"neutral":1,"section":"signaling pathways and molecules modulating cardiovascular i","type":"mentioning","typeConfidence":1,"snippet":"Purinergic signaling is highly described in tumoral context ( \u003Ccite data-doi=\"10.1111\u002Fimr.12528\"\u003E 162 \u003C\u002Fcite\u003E ) and in autoimmune diseases ( \u003Ccite data-doi=\"10.1007\u002Fs12026-016-8870-2\"\u003E 163 \u003C\u002Fcite\u003E ) but poorly studied in the context of cardiac pathologies. Given the high production rate of ATP and the turnover required to maintain its continuous mechanical work, disruption of heart tissue generates the release of high amounts of ATP to the extracellular space.","lang":"en","langConfidence":"0.9300000071525574","refLocation":"b163\u002F1","memberId":1965,"selfCites":[],"snippetHidden":false},{"id":2011390564,"source":"10.5812\u002Fhepatmon.98811","target":"10.1007\u002Fs12026-016-8870-2","negative":0.018834876269102095,"positive":0.01086360588669777,"neutral":1,"section":"introduction","type":"mentioning","typeConfidence":1,"snippet":"Adenosine is a key immunosuppressive signal in microenvironments that is generated from the degradation of ATP after being catalyzed by CD39 and CD73. Adenosine promotes regulatory T cells (Treg) proliferation and activity \u003Ccite data-doi=\"10.1007\u002Fs12026-016-8870-2\"\u003E(6)\u003C\u002Fcite\u003E. Treg cells, known as suppressor T cells, play an important role in the modulation of immune response and maintenance of immunological tolerance.","lang":"en","langConfidence":"0.9300000071525574","refLocation":"b5\u002F1","memberId":3819,"selfCites":[{"type":"SELFCITE","family":"Gao","given":"Zhao-Wei"},{"type":"SHAREDAUTHOR","family":"Dong","given":"Ke"},{"type":"SHAREDAUTHOR","family":"Zhang","given":"Hui-Zhong"}],"snippetHidden":false},{"id":2011390568,"source":"10.5812\u002Fhepatmon.98811","target":"10.1007\u002Fs12026-016-8870-2","negative":0.022424452006816864,"positive":0.02358604408800602,"neutral":1,"section":"introduction","type":"mentioning","typeConfidence":1,"snippet":"Adenosine deaminase is a key enzyme involved in the adenosine metabolism pathway, which catalyzes the deamination of adenosine \u003Ccite data-doi=\"10.1111\u002Fj.1600-065x.1998.tb01569.x\"\u003E(9)\u003C\u002Fcite\u003E. Adenosine deaminase plays an important role in the maturation and maintenance of immunological response \u003Ccite data-doi=\"10.1007\u002Fs12026-016-8870-2\"\u003E(6,\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1186\u002Fs13023-018-0807-5\"\u003E10,\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.3390\u002Fbiom5020775\"\u003E11)\u003C\u002Fcite\u003E. It has been found to be essential for lymphocytic proliferation and differentiation \u003Ccite data-doi=\"10.3389\u002Ffimmu.2016.00314\"\u003E(12)\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1189\u002Fjlb.1009696\"\u003E(13)\u003C\u002Fcite\u003E\u003Ccite data-doi=\"10.1189\u002Fjlb.1109764\"\u003E(14)\u003C\u002Fcite\u003E.","lang":"en","langConfidence":"0.8999999761581421","refLocation":"b5\u002F2","memberId":3819,"selfCites":[{"type":"SELFCITE","family":"Gao","given":"Zhao-Wei"},{"type":"SHAREDAUTHOR","family":"Dong","given":"Ke"},{"type":"SHAREDAUTHOR","family":"Zhang","given":"Hui-Zhong"}],"snippetHidden":false},{"source":"10.1002\u002Fjlb.4ma0420-125r","target":"10.1007\u002Fs12026-016-8870-2","selfCites":[],"dataSource":"CR"},{"source":"10.1007\u002F978-3-030-49270-0_10","target":"10.1007\u002Fs12026-016-8870-2","selfCites":[],"dataSource":"CR"},{"source":"10.1007\u002Fs11302-018-9628-1","target":"10.1007\u002Fs12026-016-8870-2","selfCites":[],"dataSource":"CR"},{"source":"10.1007\u002Fs11302-021-09832-4","target":"10.1007\u002Fs12026-016-8870-2","selfCites":[],"dataSource":"CR"},{"source":"10.1007\u002Fs11302-021-09838-y","target":"10.1007\u002Fs12026-016-8870-2","selfCites":[],"dataSource":"CR"}],"citationTallies":{"10.1189\u002Fjlb.5a0816-346r":{"total":43,"supporting":5,"contradicting":0,"mentioning":38,"unclassified":0,"doi":"10.1189\u002Fjlb.5a0816-346r","citingPublications":31},"10.5812\u002Fhepatmon.98811":{"total":1,"supporting":0,"contradicting":0,"mentioning":1,"unclassified":0,"doi":"10.5812\u002Fhepatmon.98811","citingPublications":3},"10.3389\u002Ffimmu.2017.01921":{"total":26,"supporting":0,"contradicting":0,"mentioning":26,"unclassified":0,"doi":"10.3389\u002Ffimmu.2017.01921","citingPublications":42},"10.3389\u002Ffimmu.2018.01322":{"total":19,"supporting":3,"contradicting":0,"mentioning":16,"unclassified":0,"doi":"10.3389\u002Ffimmu.2018.01322","citingPublications":24},"10.1002\u002Fjlb.4ma0420-125r":{"total":6,"supporting":0,"contradicting":0,"mentioning":6,"unclassified":0,"doi":"10.1002\u002Fjlb.4ma0420-125r","citingPublications":7},"10.1007\u002F978-3-030-49270-0_10":{"total":2,"supporting":0,"contradicting":0,"mentioning":2,"unclassified":0,"doi":"10.1007\u002F978-3-030-49270-0_10","citingPublications":3},"10.1007\u002Fs11302-018-9628-1":{"total":10,"supporting":0,"contradicting":0,"mentioning":10,"unclassified":0,"doi":"10.1007\u002Fs11302-018-9628-1","citingPublications":13},"10.1007\u002Fs11302-021-09832-4":{"total":1,"supporting":0,"contradicting":0,"mentioning":1,"unclassified":0,"doi":"10.1007\u002Fs11302-021-09832-4","citingPublications":4},"10.1007\u002Fs11302-021-09838-y":{"total":12,"supporting":0,"contradicting":0,"mentioning":12,"unclassified":0,"doi":"10.1007\u002Fs11302-021-09838-y","citingPublications":22}},"metadata":{"totalCitationCount":32,"restrictedCitationCount":5,"distinctSourceCount":33,"totalReferenceStatementsCount":51},"papers":{"10.1189\u002Fjlb.5a0816-346r":{"id":110139642,"doi":"10.1189\u002Fjlb.5a0816-346r","slug":"down-regulation-of-cd73-on-b-4pba0V","type":"journal-article","title":"Down-regulation of CD73 on B cells of patients with viremic HIV correlates with B cell activation and disease progression","abstract":"Recently, alterations of the T cell expression of the ectonucleotidases, CD39 and CD73, during HIV infection have been described. Here, peripheral ( = 70) and lymph nodal B cells ( = 10) of patients with HIV at different stages of disease as well as uninfected individuals were analyzed via multicolor flow cytometry with regard to expression of CD39 and CD73 and differentiation, proliferation, and exhaustion status. Patients with chronic, untreated HIV showed a significantly decreased frequency of CD73-expressing B cells ( \u003C 0.001) compared with healthy controls. Decreased frequencies of CD39CD73 B cells in patients with HIV correlated with low CD4 counts ( \u003C 0.0256) as well as increased proliferation and exhaustion status as determined by Ki-67 and programmed death-1 expression. Down-regulation of CD73 was observed in naive and memory B cells as determined by CD27 and CD21. Neither HIV elite controller patients nor antiretroviral therapy-treated patients had significantly lower CD39 and CD73 expression on B cells compared with healthy controls. Of importance, low CD73 expression on B cells was associated with modulated in vitro B cell function. Further in vivo studies are warranted to evaluate the in vivo role of phenotypic loss of CD73 in B cell dysregulation in HIV.","authors":[{"family":"Kim","given":"Eun Seong","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"eun-seong-kim-M22vRW","authorName":"Eun Seong Kim","authorID":"7707852","authorLastKnownAffiliationId":11341,"authorSequenceNumber":1,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Ackermann","given":"Christin","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"christin-ackermann-5YEDdA","authorName":"Christin Ackermann","authorID":"9589569","authorLastKnownAffiliationId":150125,"authorSequenceNumber":2,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Tóth","given":"Ilona","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"ilona-toth-ePKQDz","authorName":"Ilona Tóth","authorID":"8150755","authorLastKnownAffiliationId":177273,"authorSequenceNumber":3,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Dierks","given":"Patrick","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"patrick-dierks-6MPWzp","authorName":"Patrick Dierks","authorID":"10639798","authorLastKnownAffiliationId":203463,"authorSequenceNumber":4,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Eberhard","given":"Johanna M.","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"johanna-m-eberhard-zbpn6Y","authorName":"Johanna M. Eberhard","authorID":"8254694","authorLastKnownAffiliationId":196160,"authorSequenceNumber":5,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Wroblewski","given":"Raluca","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"raluca-wroblewski-LKkp5","authorName":"Raluca Wroblewski","authorID":"1465684","authorLastKnownAffiliationId":276938,"authorSequenceNumber":6,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Scherg","given":"Felix","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"felix-scherg-xPPj1b","authorName":"Felix Scherg","authorID":"19223266","authorLastKnownAffiliationId":150125,"authorSequenceNumber":7,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Geyer","given":"Matthias","affiliation":"Center of Advanced European Studies and Research","authorSlug":"matthias-geyer-W8lZyJ","authorName":"Matthias Geyer","authorID":"5021604","authorLastKnownAffiliationId":4863,"authorSequenceNumber":8,"affiliationSlug":"center-of-advanced-european-studies-eA9Y","affiliationID":"19199"},{"family":"Schmidt","given":"Reinhold","affiliation":"German Center for Infection Research","authorSlug":"reinhold-schmidt-YZdGO2","authorName":"Reinhold Schmidt","authorID":"4808951","authorLastKnownAffiliationId":12508,"authorSequenceNumber":9,"affiliationSlug":"german-center-for-infection-research-j6aZV","affiliationID":"240081"},{"family":"Beisel","given":"Claudia","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"claudia-beisel-M2zQVm","authorName":"Claudia Beisel","authorID":"7939596","authorLastKnownAffiliationId":240081,"authorSequenceNumber":10,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Bockhorn","given":"Maximilian","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"maximilian-bockhorn-6Oarp","authorName":"Maximilian Bockhorn","authorID":"1018098","authorLastKnownAffiliationId":212630,"authorSequenceNumber":11,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Haag","given":"Friedrich","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"friedrich-haag-zPG35","authorName":"Friedrich Haag","authorID":"985906","authorLastKnownAffiliationId":1747,"authorSequenceNumber":12,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"},{"family":"Lunzen","given":"Jan van","affiliation":"ViiV Healthcare (United Kingdom)","authorSlug":"jan-van-lunzen-Le0ayA","authorName":"Jan van Lunzen","authorID":"5058640","authorLastKnownAffiliationId":314479,"authorSequenceNumber":13,"affiliationSlug":"viiv-healthcare-united-kingdom-Kl4dJ","affiliationID":"314479"},{"family":"Wiesch","given":"Julian Schulze zur","affiliation":"University Medical Center Hamburg-Eppendorf","authorSlug":"julian-schulze-zur-wiesch-ave0b","authorName":"Julian Schulze zur Wiesch","authorID":"1009983","authorLastKnownAffiliationId":3479,"authorSequenceNumber":14,"affiliationSlug":"university-medical-center-hamburg-eppendorf-5GAgV","affiliationID":"150125"}],"keywords":["CD39","5′‐ectonucleotidase","elite controller","ADO","Ig class switch","CD39"],"year":2017,"publisher":"Oxford University Press (OUP)","issue":"5","volume":"101","page":"1263-1271","retracted":false,"memberId":286,"issns":["0741-5400","1938-3673"],"editorialNotices":[],"journalSlug":"journal-of-leukocyte-biology-vJlwN","journal":"Journal of Leukocyte Biology","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.5812\u002Fhepatmon.98811":{"id":6926974634,"doi":"10.5812\u002Fhepatmon.98811","slug":"diagnostic-value-of-serum-adenosine-OkxGPZ4","type":"journal-article","title":"Diagnostic Value of Serum Adenosine Deaminase and Its Isoenzymes for Autoimmune Liver Disease","abstract":"Background: Adenosine Deaminase (ADA) has been found to be involved in autoimmune disease progression. Objectives: We aimed to evaluate the diagnostic value of serum ADA activity in Autoimmune Liver Disease (AILD). Methods: The study included 50 AILD patients, 33 viral hepatitis patients, and 60 healthy subjects. The serum levels of total Adenosine Deaminase (tADA) and its isoenzymes (ADA1 and ADA2) were determined. The Receiver Operating Characteristic (ROC) curve analysis was used to evaluate the diagnostic performance of serum ADA activity. Results: Our results showed that the serum tADA and ADA2 levels were significantly higher in AILD patients (tADA: 19","authors":[{"family":"Gao","given":"Zhaowei","affiliation":"Air Force Medical University","authorSlug":"zhaowei-gao-JWW6A9","authorName":"Zhaowei Gao","authorID":"7696423","authorLastKnownAffiliationId":278533,"authorSequenceNumber":1,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Li","given":"Rui-Cheng","affiliation":"Air Force Medical University","authorSlug":"rui-cheng-li-3nzM02","authorName":"Rui-Cheng Li","authorID":"4351244","authorLastKnownAffiliationId":4243,"authorSequenceNumber":2,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Wang","given":"Huiping","affiliation":"Air Force Medical University","authorSlug":"huiping-wang-pn54Rj","authorName":"Huiping Wang","authorID":"5106874","authorLastKnownAffiliationId":212414,"authorSequenceNumber":3,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Ma","given":"Hongwei","affiliation":"Air Force Medical University","authorSlug":"hongwei-ma-mOllL1","authorName":"Hongwei Ma","authorID":"5578187","authorLastKnownAffiliationId":1691,"authorSequenceNumber":4,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Zhang","given":"Huizhong","affiliation":"Air Force Medical University","authorSlug":"huizhong-zhang-K6mRyG","authorName":"Huizhong Zhang","authorID":"6291935","authorLastKnownAffiliationId":177251,"authorSequenceNumber":5,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Lin","given":"Fang Yue","affiliation":"Air Force Medical University","authorSlug":"fang-yue-lin-V0pRQj","authorName":"Fang Yue Lin","authorID":"7283238","authorLastKnownAffiliationId":156653,"authorSequenceNumber":6,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Dong","given":"Ke","affiliation":"Air Force Medical University","authorSlug":"ke-dong-4LwraM","authorName":"Ke Dong","authorID":"5982186","authorLastKnownAffiliationId":275325,"authorSequenceNumber":7,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"}],"keywords":["Adenosine Deaminase","Isoenzymes","Autoimmune Liver Diseases","Viral Hepatitis","Diagnosis"],"year":2020,"shortJournal":"Hepat Mon","publisher":"Brieflands","issue":"1","volume":"20","retracted":false,"memberId":3819,"issns":["1735-143X","1735-3408"],"editorialNotices":[],"journalSlug":"hepatitis-monthly-9Obxr","journal":"Hepatitis Monthly","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.3389\u002Ffimmu.2017.01921":{"id":219131895,"doi":"10.3389\u002Ffimmu.2017.01921","slug":"new-insights-into-the-immunobiology-YZ4QGO2","type":"journal-article","title":"New Insights into the Immunobiology of Mononuclear Phagocytic Cells and Their Relevance to the Pathogenesis of Cardiovascular Diseases","abstract":"Macrophages are the primary immune cells that reside within the myocardium, suggesting that these mononuclear phagocytes are essential in the orchestration of cardiac immunity and homeostasis. Independent of the nature of the injury, the heart triggers leukocyte activation and recruitment. However, inflammation is harmful to this vital terminally differentiated organ with extremely poor regenerative capacity. As such, cardiac tissue has evolved particular strategies to increase the stress tolerance and minimize the impact of inflammation. In this sense, growing evidences show that mononuclear phagocytic cells are particularly dynamic during cardiac inflammation or infection and would actively participate in tissue repair and functional recovery. They respond to soluble mediators such as metabolites or cytokines, which play central roles in the timing of the intrinsic cardiac stress response. During myocardial infarction two distinct phases of monocyte influx have been identified. Upon infarction, the heart modulates its chemokine expression profile that sequentially and actively recruits inflammatory monocytes, first, and healing monocytes, later. In the same way, a sudden switch from inflammatory macrophages (with microbicidal effectors) toward anti-inflammatory macrophages occurs within the myocardium very shortly after infection with Trypanosoma cruzi, the causal agent of Chagas cardiomyopathy. While in sterile injury, healing response is necessary to stop tissue damage; during an intracellular infection, the anti-inflammatory milieu in infected hearts would promote microbial persistence. The balance of mononuclear phagocytic cells seems to be also dynamic in atherosclerosis influencing plaque initiation and fate. This review summarizes the participation of mononuclear phagocyte system in cardiovascular diseases, keeping in mind that the immune system evolved to promote the reestablishment of tissue homeostasis following infection\u002Finjury, and that the effects of different mediators could modulate the magnitude and quality of the immune response. The knowledge of the effects triggered by diverse mediators would serve to identify new therapeutic targets in different cardiovascular pathologies.","authors":[{"family":"Sanmarco","given":"Liliana M.","affiliation":"Universidad Nacional de Córdoba","authorSlug":"liliana-m-sanmarco-ZGKyAp","authorName":"Liliana M. Sanmarco","authorID":"7332975","authorLastKnownAffiliationId":9610,"authorSequenceNumber":1,"affiliationSlug":"universidad-nacional-de-cordoba-yVGl","affiliationID":"14620"},{"family":"Eberhardt","given":"Natalia","affiliation":"Research Centre in Biological Chemistry of Córdoba","authorSlug":"natalia-eberhardt-zbx8yb","authorName":"Natalia Eberhardt","authorID":"8082406","authorLastKnownAffiliationId":15862,"authorSequenceNumber":2,"affiliationSlug":"research-centre-in-biological-chemistry-4Zl8P","affiliationID":"267186"},{"family":"Ponce","given":"Nicolás","affiliation":"Universidad Nacional de Córdoba","authorSlug":"nicolas-ponce-6M4gv9","authorName":"Nicolás Ponce","authorID":"8956298","authorLastKnownAffiliationId":267186,"authorSequenceNumber":3,"affiliationSlug":"universidad-nacional-de-cordoba-yVGl","affiliationID":"14620"},{"family":"Cano","given":"Roxana Carolina","affiliation":"Universidad Nacional de Córdoba","authorSlug":"roxana-carolina-cano-Ea1Pr8","authorName":"Roxana Carolina Cano","authorID":"8645417","authorLastKnownAffiliationId":14620,"authorSequenceNumber":4,"affiliationSlug":"universidad-nacional-de-cordoba-yVGl","affiliationID":"14620"},{"family":"Bonacci","given":"Gustavo","affiliation":"Universidad Nacional de Córdoba","authorSlug":"gustavo-bonacci-A3kyGv","authorName":"Gustavo Bonacci","authorID":"6419949","authorLastKnownAffiliationId":267186,"authorSequenceNumber":5,"affiliationSlug":"universidad-nacional-de-cordoba-yVGl","affiliationID":"14620"},{"family":"Aoki","given":"María Pilar","affiliation":"Universidad Nacional de Córdoba","authorSlug":"maria-pilar-aoki-V0lZKW","authorName":"María Pilar Aoki","authorID":"7151682","authorLastKnownAffiliationId":267186,"authorSequenceNumber":6,"affiliationSlug":"universidad-nacional-de-cordoba-yVGl","affiliationID":"14620"}],"keywords":["Immunology"],"year":2018,"shortJournal":"Front. Immunol.","publisher":"Frontiers Media SA","volume":"8","retracted":false,"memberId":1965,"issns":["1664-3224"],"editorialNotices":[],"journalSlug":"frontiers-in-immunology-pnD8b","journal":"Frontiers in Immunology","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.3389\u002Ffimmu.2018.01322":{"id":221543670,"doi":"10.3389\u002Ffimmu.2018.01322","slug":"ectonucleotidase-mediated-suppression-of-lupus-autoimmunity-RVaZP6G","type":"journal-article","title":"Ectonucleotidase-Mediated Suppression of Lupus Autoimmunity and Vascular Dysfunction","abstract":"ObjectivesCD39 and CD73 are surface enzymes that jut into the extracellular space where they mediate the step-wise phosphohydrolysis of the autocrine and paracrine danger signals ATP and ADP into anti-inflammatory adenosine. Given the role of vascular and immune cells’ “purinergic halo” in maintaining homeostasis, we hypothesized that the ectonucleotidases CD39 and CD73 might play a protective role in lupus.MethodsLupus was modeled by intraperitoneal administration of pristane to three groups of mice: wild-type (WT), CD39−\u002F−, and CD73−\u002F−. After 36 weeks, autoantibodies, endothelial function, kidney disease, splenocyte activation\u002Fpolarization, and neutrophil activation were characterized.ResultsAs compared with WT mice, CD39−\u002F− mice developed exaggerated splenomegaly in response to pristane, while both groups of ectonucleotidase-deficient mice demonstrated heightened anti-ribonucleoprotein production. The administration of pristane to WT mice triggered only subtle dysfunction of the arterial endothelium; however, both CD39−\u002F− and CD73−\u002F− mice demonstrated striking endothelial dysfunction following induction of lupus, which could be reversed by superoxide dismutase. Activated B cells and plasma cells were expanded in CD73−\u002F− mice, while deficiency of either ectonucleotidase led to expansion of TH17 cells. CD39−\u002F− and CD73−\u002F− mice demonstrated exaggerated neutrophil extracellular trap release, while CD73−\u002F− mice additionally had higher levels of plasma cell-free DNA.ConclusionThese data are the first to link ectonucleotidases with lupus autoimmunity and vascular disease. New therapeutic strategies may harness purinergic nucleotide dissipation or signaling to limit the damage inflicted upon organs and blood vessels by lupus.","authors":[{"family":"Knight","given":"Jason S.","affiliation":"University of Michigan–Ann Arbor","authorSlug":"jason-s-knight-xXeKpg","authorName":"Jason S. Knight","authorID":"5920666","authorLastKnownAffiliationId":5792,"authorSequenceNumber":1,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Mazza","given":"Levi F.","affiliation":"University of Michigan–Ann Arbor","authorSlug":"levi-f-mazza-2N5mrx","authorName":"Levi F. Mazza","authorID":"7031976","authorLastKnownAffiliationId":158401,"authorSequenceNumber":2,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Yalavarthi","given":"Srilakshmi","affiliation":"University of Michigan–Ann Arbor","authorSlug":"srilakshmi-yalavarthi-ZG4Rpd","authorName":"Srilakshmi Yalavarthi","authorID":"5154675","authorLastKnownAffiliationId":5792,"authorSequenceNumber":3,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Sule","given":"Gautam","affiliation":"University of Michigan–Ann Arbor","authorSlug":"gautam-sule-rx630A","authorName":"Gautam Sule","authorID":"7646829","authorLastKnownAffiliationId":5792,"authorSequenceNumber":4,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Ali","given":"Ramadan A.","affiliation":"University of Michigan–Ann Arbor","authorSlug":"ramadan-a-ali-LD5zwa","authorName":"Ramadan A. Ali","authorID":"7507340","authorLastKnownAffiliationId":1013,"authorSequenceNumber":5,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Hodgin","given":"Jeffrey B.","affiliation":"University of Michigan–Ann Arbor","authorSlug":"jeffrey-b-hodgin-1XeK0","authorName":"Jeffrey B. Hodgin","authorID":"974247","authorLastKnownAffiliationId":5792,"authorSequenceNumber":6,"affiliationSlug":"university-of-michigan-ann-arbor-WG91","affiliationID":"5792"},{"family":"Kanthi","given":"Yogendra","affiliation":"VA Ann Arbor Healthcare System","authorSlug":"yogendra-kanthi-K6GMdJ","authorName":"Yogendra Kanthi","authorID":"5775935","authorLastKnownAffiliationId":283916,"authorSequenceNumber":7,"affiliationSlug":"va-ann-arbor-healthcare-system-5Y88G","affiliationID":"239669"},{"family":"Pinsky","given":"David J.","affiliation":"Michigan Medicine","authorSlug":"david-j-pinsky-dv5dmy","authorName":"David J. Pinsky","authorID":"5813262","authorLastKnownAffiliationId":5792,"authorSequenceNumber":8,"affiliationSlug":"michigan-medicine-4ZEWM","affiliationID":"284142"}],"keywords":["Immunology"],"year":2018,"shortJournal":"Front. Immunol.","publisher":"Frontiers Media SA","volume":"9","retracted":false,"memberId":1965,"issns":["1664-3224"],"editorialNotices":[],"journalSlug":"frontiers-in-immunology-pnD8b","journal":"Frontiers in Immunology","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.1002\u002Fjlb.4ma0420-125r":{"id":9362469458,"doi":"10.1002\u002Fjlb.4ma0420-125r","slug":"hif-1α-and-cd73-expression-in-gZLxW5L5","type":"journal-article","title":"HIF-1α and CD73 expression in cardiac leukocytes correlates with the severity of myocarditis in end-stage Chagas disease patients","abstract":"Chronic Chagas cardiomyopathy is the main infectious myocarditis worldwide. Almost 30% of Trypanosoma cruzi infected individuals develop slow and progressive myocarditis that leads to ventricular dilation and heart failure. Heart transplantation is an established, valuable therapeutic option for end-stage Chagas disease patients. Although the pathophysiology of Chagas disease has been addressed for decades by numerous groups, the cardiac immunologic mechanisms involved in the progression of clinical manifestation are still unknown. Growing evidence demonstrates that hypoxia-inducible factor (HIF)-1 plays indispensable roles in driving immune response by triggering the expression of CD73 purinergic ecto-enzyme. Purinergic system controls the duration and magnitude of purine signals directed to modulate immune cells through the conversion of extracellular ATP (microbicide\u002Fproinflammatory) to the immunoregulatory metabolite adenosine. In the present work, we described that infiltrating leukocytes within cardiac explants from patients with end-stage Chagas cardiomyopathy up-regulated HIF-1 and CD73 expression. Moreover, the number of HIF-1 + and CD73+ leukocytes positively correlated with the myocarditis severity and the local parasite load. Furthermore, we demonstrated a direct relationship between tissue parasite persistence and the influx of immune cells to the infected hearts, which ultimately determine the severity of the myocarditis. These findings provide evidence that CD73-dependent regulatory pathways are locally triggered in the myocardium of patients with end-stage Chagas disease.","authors":[{"family":"Eberhardt","given":"Natalia","affiliation":"Research Centre in Biological Chemistry of Córdoba","authorSlug":"natalia-eberhardt-zbx8yb","authorName":"Natalia Eberhardt","authorID":"8082406","authorLastKnownAffiliationId":15862,"authorSequenceNumber":1,"affiliationSlug":"research-centre-in-biological-chemistry-4Zl8P","affiliationID":"267186"},{"family":"Sanmarco","given":"Liliana M.","affiliation":"Research Centre in Biological Chemistry of Córdoba","authorSlug":"liliana-m-sanmarco-ZGKyAp","authorName":"Liliana M. Sanmarco","authorID":"7332975","authorLastKnownAffiliationId":9610,"authorSequenceNumber":2,"affiliationSlug":"research-centre-in-biological-chemistry-4Zl8P","affiliationID":"267186"},{"family":"Bergero","given":"Gastón","affiliation":"Research Centre in Biological Chemistry of Córdoba","authorSlug":"gaston-bergero-MlavXX","authorName":"Gastón Bergero","authorID":"15289852","authorLastKnownAffiliationId":267186,"authorSequenceNumber":3,"affiliationSlug":"research-centre-in-biological-chemistry-4Zl8P","affiliationID":"267186"},{"family":"Favaloro","given":"Roberto","affiliation":"Fundacion Favaloro Hospital Universitario","authorSlug":"roberto-favaloro-xXjmPA","authorName":"Roberto Favaloro","authorID":"6247722","authorLastKnownAffiliationId":170333,"authorSequenceNumber":4,"affiliationSlug":"fundacion-favaloro-hospital-universitario-ePwMK","affiliationID":"219655"},{"family":"Vigliano","given":"Carlos","affiliation":"Consejo Nacional de Investigaciones Científicas y Técnicas","authorSlug":"carlos-vigliano-1Zy3yW","authorName":"Carlos Vigliano","authorID":"6120891","authorLastKnownAffiliationId":219655,"authorSequenceNumber":5,"affiliationSlug":"consejo-nacional-de-investigaciones-cientificas-Qrbw","affiliationID":"14160"},{"family":"Aoki","given":"María Pilar","affiliation":"Research Centre in Biological Chemistry of Córdoba","authorSlug":"maria-pilar-aoki-V0lZKW","authorName":"María Pilar Aoki","authorID":"7151682","authorLastKnownAffiliationId":267186,"authorSequenceNumber":6,"affiliationSlug":"research-centre-in-biological-chemistry-4Zl8P","affiliationID":"267186"}],"keywords":["cardiomyopathy","hypoxia","purinergic system","T-cells","T. cruzi infection"],"year":2020,"publisher":"Oxford University Press (OUP)","issue":"1","volume":"109","page":"233-244","retracted":false,"memberId":286,"issns":["0741-5400","1938-3673"],"editorialNotices":[],"journalSlug":"journal-of-leukocyte-biology-vJlwN","journal":"Journal of Leukocyte Biology","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.1007\u002F978-3-030-49270-0_10":{"id":9775641169,"doi":"10.1007\u002F978-3-030-49270-0_10","slug":"b-cells-in-the-gastrointestinal-5Gjd6R9V","type":"book-chapter","title":"B Cells in the Gastrointestinal Tumor Microenvironment with a Focus on Pancreatic Cancer: Opportunities for Precision Medicine?","authors":[{"family":"Ligeiro","given":"Dário","authorSlug":"dario-ligeiro-arMdj","authorName":"Dário Ligeiro","authorID":"2376883","authorLastKnownAffiliationId":199260,"authorSequenceNumber":1},{"family":"Rao","given":"Martin","affiliation":"Champalimaud Foundation","authorSlug":"martin-rao-vJYwOW","authorName":"Martin Rao","authorID":"6494653","authorLastKnownAffiliationId":16338,"authorSequenceNumber":2,"affiliationSlug":"champalimaud-foundation-VL6O","affiliationID":"16338"},{"family":"Maia","given":"Andreia","affiliation":"Champalimaud Foundation","authorSlug":"andreia-maia-LyZ8r","authorName":"Andreia Maia","authorID":"3513784","authorLastKnownAffiliationId":16338,"authorSequenceNumber":3,"affiliationSlug":"champalimaud-foundation-VL6O","affiliationID":"16338"},{"family":"Castillo","given":"Maurício","affiliation":"Champalimaud Foundation","authorSlug":"mauricio-castillo-pn5zdw","authorName":"Maurício Castillo","authorID":"5076774","authorLastKnownAffiliationId":163030,"authorSequenceNumber":4,"affiliationSlug":"champalimaud-foundation-VL6O","affiliationID":"16338"},{"family":"Beltrán","given":"Antonio","affiliation":"Champalimaud Foundation","authorSlug":"antonio-beltran-mORAM2","authorName":"Antonio Beltrán","authorID":"6231743","authorLastKnownAffiliationId":16338,"authorSequenceNumber":5,"affiliationSlug":"champalimaud-foundation-VL6O","affiliationID":"16338"},{"family":"Maeurer","given":"Markus","affiliation":"Champalimaud Foundation","authorSlug":"markus-maeurer-OVDK66","authorName":"Markus Maeurer","authorID":"5826234","authorLastKnownAffiliationId":25299,"authorSequenceNumber":6,"affiliationSlug":"champalimaud-foundation-VL6O","affiliationID":"16338"}],"year":2020,"publisher":"Springer International Publishing","page":"175-195","memberId":297,"issns":["0065-2598","2214-8019"],"editorialNotices":[],"journal":"Advances in Experimental Medicine and Biology","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["book"]},"10.1007\u002Fs11302-018-9628-1":{"id":245351561,"doi":"10.1007\u002Fs11302-018-9628-1","slug":"multiple-steps-determine-cd73-shedding-EWPlN2y","type":"journal-article","title":"Multiple steps determine CD73 shedding from RPE: lipid raft localization, ARA1 interaction, and MMP-9 up-regulation","abstract":"Physiologically, retinal pigment epithelium (RPE) expresses high levels of CD73 in their membrane, converting AMP to immune suppressive adenosine, mediates an anti-inflammatory effect. However, after being exposed to inflammatory factors, RPE rapidly becomes CD73-negative cells, which render RPE's immune suppressive function and accelerate local inflammation. Here, we investigated the mechanism leading to the loss of membrane CD73 in RPE. We found the controversy that when membrane CD73 was significantly diminished in inflammatory RPE, Cd73 mRNA levels were not changed at all. It was further verified that, matrix metalloproteinase-9 (MMP-9) mediated the shedding of CD73 from the cell membrane of inflammatory RPE by catalyzing its K547\u002FF548 site. However, MMP-9 could not catalyze uncomplexed CD73, the interaction of CD73 with adenosine receptor A1 subtype (ARA1) is necessary for being catalyzed by MMP-9. After being treated by LPS and TNF-α, the formation of CD73\u002FARA1 complex in RPE was verified by co-immunoprecipitation and FRET-based assays. It was also revealed that CD73 need to be localized in lipid rafts to be capable of interacting with ARA1, since CD73\u002FARA1 interaction and CD73 shedding were completely blocked by the addition of lipid raft synthesis inhibitor. As a conclusion, multiple steps are involved in CD73 shedding in RPE, including up-regulation of MMP-9 activity, localization of CD73 in lipid rafts, and the formation of CD73\u002FARA1 complex. Lipid rafts committed CD73 with high mobility, shuttled CD73 to ARA1 to form a complex, which was capable of being recognized and catalyzed by MMP-9.","authors":[{"family":"Zhang","given":"Wei","affiliation":"Tianjin Medical University Eye Hospital","authorSlug":"wei-zhang-mOK6Xg","authorName":"Wei Zhang","authorID":"5700087","authorLastKnownAffiliationId":275254,"authorSequenceNumber":1,"affiliationSlug":"tianjin-medical-university-eye-hospital-5Y98Q","affiliationID":"206769"},{"family":"Zhou","given":"Shumin","affiliation":"Tianjin Medical University","authorSlug":"shumin-zhou-aXG5bv","authorName":"Shumin Zhou","authorID":"6193583","authorLastKnownAffiliationId":196523,"authorSequenceNumber":2,"affiliationSlug":"tianjin-medical-university-EVnP","affiliationID":"23517"},{"family":"Liu","given":"Shuai","affiliation":"Tianjin First Center Hospital","authorSlug":"shuai-liu-dvLynj","authorName":"Shuai Liu","authorID":"4822218","authorLastKnownAffiliationId":12338,"authorSequenceNumber":3,"affiliationSlug":"tianjin-first-center-hospital-mD5X","affiliationID":"8987"},{"family":"Kong","given":"Fanting","affiliation":"Tianjin Medical University General Hospital","authorSlug":"fanting-kong-9O1MPk","authorName":"Fanting Kong","authorID":"6291890","authorLastKnownAffiliationId":16090,"authorSequenceNumber":4,"affiliationSlug":"tianjin-medical-university-general-hospital-ZjWd","affiliationID":"13275"},{"family":"Song","given":"Chao","affiliation":"Tianjin Medical University General Hospital","authorSlug":"chao-song-MVOyJY","authorName":"Chao Song","authorID":"5977708","authorLastKnownAffiliationId":151072,"authorSequenceNumber":5,"affiliationSlug":"tianjin-medical-university-general-hospital-ZjWd","affiliationID":"13275"},{"family":"Yan","given":"Hua","affiliation":"Tianjin Medical University General Hospital","authorSlug":"hua-yan-vJOEav","authorName":"Hua Yan","authorID":"6293609","authorLastKnownAffiliationId":216536,"authorSequenceNumber":6,"affiliationSlug":"tianjin-medical-university-general-hospital-ZjWd","affiliationID":"13275"}],"keywords":["CD73","Shedding","Lipid rafts","MMP-9","Adenosine receptor A1"],"year":2018,"shortJournal":"Purinergic Signalling","publisher":"Springer Science and Business Media LLC","issue":"4","volume":"14","page":"443-457","retracted":false,"memberId":297,"issns":["1573-9538","1573-9546"],"editorialNotices":[],"journalSlug":"purinergic-signalling-zRYL3","journal":"Purinergic Signalling","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.1007\u002Fs11302-021-09832-4":{"id":11289133253,"doi":"10.1007\u002Fs11302-021-09832-4","slug":"mono-adp-ribosylation-sites-of-human-cd73-vJ6nmnEV","type":"journal-article","title":"Mono-ADP-ribosylation sites of human CD73 inhibit its adenosine-generating enzymatic activity","abstract":"CD73-derived adenosine plays a major role in damage-induced tissue responses by inhibiting inflammation. Damage-associated stimuli, such as hypoxia and mechanical stress, induce the cellular release of ATP and NAD+ and upregulate the expression of the nucleotide-degrading purinergic ectoenzyme cascade, including adenosine-generating CD73. Extracellular NAD+ also serves as substrate for mono-ADP-ribosylation of cell surface proteins, which in human cells is mediated by ecto-ADP-ribosyltransferase 1 (ARTC1). Here we explored, whether human CD73 enzymatic activity is regulated by mono-ADP-ribosylation, using recombinant human CD73 in the presence of ARTC1 with etheno-labelled NAD+ as substrate. Multi-colour immunoblotting with an anti-etheno-adenosine antibody showed ARTC1-mediated transfer of ADP-ribose together with the etheno label to CD73. HPLC analysis of the enzymatic activity of in vitro-ribosylated CD73 revealed strong inhibition of adenosine generation in comparison to non-ribosylated CD73. Mass spectrometry of in vitro-ribosylated CD73 identified six ribosylation sites. 3D model analysis indicated that three of them (R328, R354, R545) can interfere with CD73 enzymatic activity. Our study identifies human CD73 as target for ARTC1-mediated mono-ADP-ribosylation, which can profoundly modulate its adenosine-generating activity. Thus, in settings with enhanced release of NAD+ as substrate for ARTC1, assessment of CD73 protein expression in human tissues may not be predictive of adenosine formation resulting in anti-inflammatory activity.","authors":[{"family":"Hesse","given":"Julia","affiliation":"Heinrich Heine University Düsseldorf","authorSlug":"julia-hesse-lX1dvy","authorName":"Julia Hesse","authorID":"9056436","authorLastKnownAffiliationId":7439,"authorSequenceNumber":1,"affiliationSlug":"heinrich-heine-university-dusseldorf-ajej","affiliationID":"7439"},{"family":"Rosse","given":"Mona K","affiliation":"Heinrich Heine University Düsseldorf","authorSlug":"mona-k-rosse-Z3MblM","authorName":"Mona K Rosse","authorID":"18681431","authorLastKnownAffiliationId":7439,"authorSequenceNumber":2,"affiliationSlug":"heinrich-heine-university-dusseldorf-ajej","affiliationID":"7439"},{"family":"Steckel","given":"Bodo","affiliation":"Heinrich Heine University Düsseldorf","authorSlug":"bodo-steckel-wmOGKa","authorName":"Bodo Steckel","authorID":"6269772","authorLastKnownAffiliationId":7439,"authorSequenceNumber":3,"affiliationSlug":"heinrich-heine-university-dusseldorf-ajej","affiliationID":"7439"},{"family":"Blank-Landeshammer","given":"Bernhard","affiliation":"Leibniz Institute for Analytical Sciences - ISAS","authorSlug":"bernhard-blank-landeshammer-xQY9JM","authorName":"Bernhard Blank-Landeshammer","authorID":"9234666","authorLastKnownAffiliationId":156041,"authorSequenceNumber":4,"affiliationSlug":"leibniz-institute-for-analytical-sciences-DxnNp","affiliationID":"202719"},{"family":"Idel","given":"Svenja","affiliation":"Leibniz Institute for Analytical Sciences - ISAS","authorSlug":"svenja-idel-8Adbm","authorName":"Svenja Idel","authorID":"1571465","authorLastKnownAffiliationId":202719,"authorSequenceNumber":5,"affiliationSlug":"leibniz-institute-for-analytical-sciences-DxnNp","affiliationID":"202719"},{"family":"Reinders","given":"Yvonne","affiliation":"Leibniz Institute for Analytical Sciences - ISAS","authorSlug":"yvonne-reinders-j6jy6d","authorName":"Yvonne Reinders","authorID":"8334581","authorLastKnownAffiliationId":202938,"authorSequenceNumber":6,"affiliationSlug":"leibniz-institute-for-analytical-sciences-DxnNp","affiliationID":"202719"},{"family":"Sickmann","given":"Albert","affiliation":"Leibniz Institute for Analytical Sciences - ISAS","authorSlug":"albert-sickmann-zRdmbK","authorName":"Albert Sickmann","authorID":"4909806","authorLastKnownAffiliationId":202938,"authorSequenceNumber":7,"affiliationSlug":"leibniz-institute-for-analytical-sciences-DxnNp","affiliationID":"202719"},{"family":"Sträter","given":"Norbert","affiliation":"Leipzig University","authorSlug":"norbert-strater-J12paw","authorName":"Norbert Sträter","authorID":"5177023","authorLastKnownAffiliationId":7595,"authorSequenceNumber":8,"affiliationSlug":"leipzig-university-YDpr","affiliationID":"7595"},{"family":"Schrader","given":"Jürgen","affiliation":"Heinrich Heine University Düsseldorf","authorSlug":"jurgen-schrader-3n5n4g","authorName":"Jürgen Schrader","authorID":"4943944","authorLastKnownAffiliationId":256313,"authorSequenceNumber":9,"affiliationSlug":"heinrich-heine-university-dusseldorf-ajej","affiliationID":"7439"}],"keywords":["Mono-ADP-ribosylation","Post-translational modification","NT5e","CD296","Adenosine"],"year":2021,"shortJournal":"Purinergic Signalling","publisher":"Springer Science and Business Media LLC","issue":"1","volume":"18","page":"115-121","memberId":297,"issns":["1573-9538","1573-9546"],"editorialNotices":[],"journalSlug":"purinergic-signalling-zRYL3","journal":"Purinergic Signalling","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.1007\u002Fs11302-021-09838-y":{"id":11296096352,"doi":"10.1007\u002Fs11302-021-09838-y","slug":"purinergic-modulation-of-the-immune-MVEvk0DE","type":"journal-article","title":"Purinergic modulation of the immune response to infections","abstract":"Infectious diseases are caused by the invasion of pathogenic microorganisms such as fungi, bacteria, viruses, and parasites. After infection, disease progression relies on the complex interplay between the host immune response and the microorganism evasion strategies. The host’s survival depends on its ability to mount an efficient protective anti-microbial response to accomplish pathogen clearance while simultaneously preventing tissue injury by keeping under control the excessive inflammatory process. The purinergic system has the dual function of regulating the immune response and triggering effector antimicrobial mechanisms. This review provides an overview of the current knowledge of the modulation of innate and adaptive immunity driven by the purinergic system during parasitic, bacterial and viral infections.","authors":[{"family":"Eberhardt","given":"Natalia","affiliation":"Consejo Nacional de Investigaciones Científicas y Técnicas","authorSlug":"natalia-eberhardt-zbx8yb","authorName":"Natalia Eberhardt","authorID":"8082406","authorLastKnownAffiliationId":15862,"authorSequenceNumber":1,"affiliationSlug":"consejo-nacional-de-investigaciones-cientificas-Qrbw","affiliationID":"14160"},{"family":"Bergero","given":"Gastón","affiliation":"Consejo Nacional de Investigaciones Científicas y Técnicas","authorSlug":"gaston-bergero-MlavXX","authorName":"Gastón Bergero","authorID":"15289852","authorLastKnownAffiliationId":267186,"authorSequenceNumber":2,"affiliationSlug":"consejo-nacional-de-investigaciones-cientificas-Qrbw","affiliationID":"14160"},{"family":"Mariotta","given":"Yanina L. Mazzocco","affiliation":"Consejo Nacional de Investigaciones Científicas y Técnicas","authorSlug":"yanina-l-mazzocco-mariotta-XEQd8A","authorName":"Yanina L. Mazzocco Mariotta","authorID":"21405985","authorLastKnownAffiliationId":14620,"authorSequenceNumber":3,"affiliationSlug":"consejo-nacional-de-investigaciones-cientificas-Qrbw","affiliationID":"14160"},{"family":"Aoki","given":"María Pilar","affiliation":"Consejo Nacional de Investigaciones Científicas y Técnicas","authorSlug":"maria-pilar-aoki-V0lZKW","authorName":"María Pilar Aoki","authorID":"7151682","authorLastKnownAffiliationId":267186,"authorSequenceNumber":4,"affiliationSlug":"consejo-nacional-de-investigaciones-cientificas-Qrbw","affiliationID":"14160"}],"keywords":["\n Review Article\n "],"year":2022,"shortJournal":"Purinergic Signalling","publisher":"Springer Science and Business Media LLC","issue":"1","volume":"18","page":"93-113","memberId":297,"issns":["1573-9538","1573-9546"],"editorialNotices":[],"journalSlug":"purinergic-signalling-zRYL3","journal":"Purinergic Signalling","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]},"10.1007\u002Fs12026-016-8870-2":{"id":61237108,"doi":"10.1007\u002Fs12026-016-8870-2","slug":"the-role-of-adenosinergic-pathway-MmRgpW","type":"journal-article","title":"The role of adenosinergic pathway in human autoimmune diseases","abstract":"Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases.","authors":[{"family":"Dong","given":"Ke","affiliation":"Air Force Medical University","authorSlug":"ke-dong-4LwraM","authorName":"Ke Dong","authorID":"5982186","authorLastKnownAffiliationId":275325,"authorSequenceNumber":1,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Gao","given":"Zhaowei","affiliation":"Air Force Medical University","authorSlug":"zhaowei-gao-JWW6A9","authorName":"Zhaowei Gao","authorID":"7696423","authorLastKnownAffiliationId":278533,"authorSequenceNumber":2,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"},{"family":"Zhang","given":"Huizhong","affiliation":"Air Force Medical University","authorSlug":"huizhong-zhang-K6mRyG","authorName":"Huizhong Zhang","authorID":"6291935","authorLastKnownAffiliationId":177251,"authorSequenceNumber":3,"affiliationSlug":"air-force-medical-university-jQpV","affiliationID":"14581"}],"keywords":["Review"],"year":2016,"shortJournal":"Immunol Res","publisher":"Springer Science and Business Media LLC","issue":"5-6","volume":"64","page":"1133-1141","retracted":false,"memberId":297,"issns":["0257-277X","1559-0755"],"editorialNotices":[],"journalSlug":"immunologic-research-A3w92","journal":"Immunologic Research","preprintLinks":[],"publicationLinks":[],"normalizedTypes":["article"]}},"tallies":{"10.1007\u002Fs12026-016-8870-2":{"total":31,"supporting":2,"contradicting":0,"mentioning":25,"unclassified":4,"doi":"10.1007\u002Fs12026-016-8870-2","citingPublications":33}},"selectCitation":null,"references":[],"referencesTotalCount":54,"referencePapers":{},"referenceTallies":{},"referencesByPapers":[],"paperLoadTracker":{"state":"loaded","key":"the-role-of-adenosinergic-pathway-MmRgpW"},"citingCountsLoadTracker":{"state":"loading"},"citationsLoadTracker":{"state":"loaded"},"referencesLoadTracker":{"state":"loaded"},"claimPaperLoadTracker":{},"flagCitationLoadTracker":{},"filters":{"showMobile":false,"sort":{"id":"relevancy","value":null,"label":"Relevance"},"supporting":null,"mentioning":null,"contradicting":null,"unclassified":null,"selfCite":null,"independent":null,"publishedRange":null,"citationsPerPage":10,"currentPage":1,"textMatch":"","citationIDs":[],"sourceDOIIDs":[],"withCitationStatements":true,"withoutCitationStatements":true,"journals":[],"authors":[],"pubtypes":[],"sections":[],"showReferences":false},"flag":{"citation":null,"citationType":null,"type":"","comment":""},"moreLikeThisResults":null,"moreLikeThisLoading":false,"exportReportLoading":false},"loginModal":{"mode":"login","name":{"placeholder":"Full Name","type":"text","value":""},"email":{"type":"email","placeholder":"Email","value":""},"password":{"type":"password","placeholder":"Password","value":""},"repeatPassword":{"type":"password","placeholder":"Repeat Password","value":""},"privacyAgreed":false,"loading":false,"userSignupType":null,"userSignupTypeLoading":false,"userSignupTypeEmail":null,"userSignupTypeOrg":null,"userSignupTypeEmailDomains":null,"fetchedSignupType":false,"fetchedSignupTypeError":false}}</script><script id="__LOADABLE_REQUIRED_CHUNKS__" type="application/json">[]</script><script id="__LOADABLE_REQUIRED_CHUNKS___ext" type="application/json">{"namedChunks":[]}</script><script async="" data-chunk="main" src="https://cdn.scite.ai/assets/dist/main.33b6f5c40898cc5cded7.js"></script><div><script id="profitwell-js" data-pw-auth="eba7f4438ac9b91fc798c9620e35aa80"> (function(i,s,o,g,r,a,m){i[o]=i[o]||function(){(i[o].q=i[o].q||[]).push(arguments)}; 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