Editorial Board Members - Journal of Molecular Immunology

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src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-mark-zabel-18914.jpg" alt="Mark D Zabel" title="Mark D Zabel" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/mark_d_zabel/"><strong>Mark Zabel</strong></a><br /> Immunology and Pathology <br /> College of Veterinary Medicine and Biomedical Sciences <br /> <a href="https://www.omicsonline.org/universities/Colorado_State_University/ ">Colorado State University</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Colorado_State_University/" target="_blank" title="Colorado State University">Colorado State University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Mark Zabel established his prion research laboratory at CSU ten years ago and is currently tenured Associate Professor and Associate Director of the PRC. He received his PhD in experimental pathology from the University of Utah. Dr. Zabel was awarded the prestigious Human Frontiers in Science Long Term Research Fellowship and received postdoctoral training in prion biology, biochemistry and pathology from the laboratory of Dr. Adriano Aguzzi at the Neuropathology Institute, University Hospital of Zürich. He also received training in immunology in the laboratory of Nobel Prize winner Dr. Rolf Zinkernagel in the Immunology Department, also at the University Hospital of Zürich. The Zabel laboratory employs molecular biological, immunological and biochemical techniques to explore peripheral pathogenesis, therapeutics and vaccines for prion diseases. Studying basic mechanisms of prion infection and dissemination provides translational information leading to diagnostic, therapeutic and vaccine targets. Dr. Zabel’s research program focuses on the interaction of prions with cells and receptors of the immune system and lymphoid tissues in the early entry, trafficking, and pathogenesis phases of prion infections. He utilizes novel mouse models of Chronic Wasting Disease that have led to numerous publications detailing translational knowledge about the role of the Complement system in prion replication, disease progression and transmission. Dr. Zabel’s laboratory currently collaborates with researchers from Fort Collins, the Front Range of Colorado, Wyoming, Nebraska, Montana, Ohio, Tennessee, Massachusetts, England, Scotland, Germany, Switzerland and Australia. Dr. Zabel received the Univeristy of Utah Molecular Biology and Biochemistry Distinguished Alumni Award in 2010 and is an Academic Editor for PLoS One. Dr. Zabel has also distinguished himself as a meeting organizer and session chair at the Regional Rocky Mountain Prion Research Symposium, Fort Collins (2008), and the International Transmissible Spongiform Encephalopathy workshops in Montreal, Canada (2011) and Amsterdam, the Netherlands (2012). His research is funded through USDA-APHIS and NIH-Neurological Disorders and Stroke."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Interaction of prions with cells and receptors of the immune system and lymphoid tissues in the early entry, trafficking, and pathogenesis phases of prion infections"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_mark_zabel.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-amy-l.-macneill-18921.jpg" alt="Amy L. MacNeill" title="Amy L. MacNeill" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/amy_l_mac_neill/"><strong>Amy L. MacNeill</strong></a><br /> Department of Microbiology, Immunology and Pathology<br /> College of Veterinary Medicine and Biomedical Sciences<br /> <a href="https://www.omicsonline.org/universities/Colorado_State_University/ ">Colorado State University</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Colorado_State_University/" target="_blank" title="Colorado State University">Colorado State University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Amy MacNeill graduated from the University of Florida College of Veterinary Medicine in 1998. Following a year in private practice, she returned to the University of Florida College of Medicine to pursue a Ph.D. mentored by Dr. Richard Moyer. Concurrently, she trained as a clinical pathology resident under Drs. John Harvey, Rose Raskin, and Rick Alleman. She became an ACVP Diplomate in 2004. Her doctoral thesis "Alterations of poxvirus serpins have unexpected effects on virus pathogenesis" was completed in 2005. Amy started her career as a clinical pathologist at the University of Illinois College of Veterinary Medicine in 2005. In 2014, she became an Associate Professor in the Department of Microbiology, Immunology, and Pathology at Colorado State University. Her current position involves clinical service, resident and student training, and medical research. Her research interests are oncology, poxvirus pathogenesis, and the use of poxviruses as vaccine vectors and oncolytic agents."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Immunology"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_amy_l_mac_neill.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-jianxun-(jim)-song-18917.jpg" alt="Jianxun (Jim) Song" title="Jianxun (Jim) Song" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/jianxun_jim_song/"><strong>Jianxun (Jim) Song</strong></a><br /> Department of Microbiology & Immunology<br /> <a href="https://www.omicsonline.org/universities/Pennsylvania_State_University/ ">The Pennsylvania State University</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Pennsylvania_State_University/" target="_blank" title="Pennsylvania State University">Pennsylvania State University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Jianxun (Jim) Song is a tenured associate professor in the Department of Microbiology and Immunology, the Pennsylvania State University College of Medicine, United States. The base of expertise on T cell biology needed to perform his research began to develop while he was a postdoctoral scholar and research scientist from the years 2001-2007 under the mentorship of Dr. Michael Croft at the La Jolla Institute for Allergy and Immunology. He became a junior faculty at The Pennsylvania State University College of Medicine in 2007, and extended his research on Developmental Immunology and Stem Cell Biology. As a PI on previous university-, foundation-, or NIH-funded grants, he laid the groundwork for the research by developing highly reactive T lymphocytes from pluripotent stem cells (PSC). His laboratory was the first to show that induced PSC differentiate into functional T cells for cell-based therapies. In addition to having the expertise to be successful with the research, he offers leadership and administrative skills that were developed during his independence as a mentor of graduate students and postdoctoral scholars. In summary, he has a demonstrated record of successful and productive research projects in the area."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Costimulation in T lymphocyte memory Regulation of differentiation of T lymphocytes from pluripotent stem cells"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_jianxun_jim_song.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-wen-hai-shao-19049.jpg" alt="Wen-Hai Shao" title="Wen-Hai Shao" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/Wen_Hai_Shao/"><strong>Wen Hai Shao</strong></a><br /> Section of Rheumatology<br /> Department of Medicine<br /> <a href="https://www.omicsonline.org/universities/Temple_University/ ">Temple University</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Temple_University/" target="_blank" title="Temple University">Temple University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Shao received his MS at Wuhan Institute of Virology (WIV), Chinese Academy of Sciences. He then moved to University of Louisville in Kentucky, USA, where he graduated with a Ph.D. in immunology. Dr. Shao started his postdoc research at the University of Pennsylvania under Dr. Philip Cohen in the area of autoimmunity. Dr. Shao moved to Temple University in 2008 and continued his research studying the molecular basis and pathogenesis of lupus and lupus nephritis using TAM- (Tyro3, Axl, Mer) deficient mice. He was appointed the Assistant Professor of Medicine in 2010."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="MY research interest is to elucidate the mechanisms that underlie the regulation of autoimmune responses and the homeostatic control of inflammation. I have discovered that the Mer receptor tyrosine kinase mediates renal protection in nephrotoxic serum-induced glomerulonephritis. I am currently unraveling the molecular and cellular determinants that account for the TAM-kinase (Tyro3, Axl, Mer) mediated regulation of renal inflammation. Recently, we found that Stat1 deficient mice develop strikingly prolonged, severe autoimmune disease when used as host in Bm12-to-B6 chronic graft-versus-host disease cGVHD, with increased autoantibody production and severe nephritis. I am exploring the aberrant signaling brought about by the absence of Stat1 to deduce its importance as a key regulator in autoimmune renal inflammation."> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_wen_hai_shao.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-alexander-y.-tsygankov-19051.jpg" alt="Alexander Y. Tsygankov" title="Alexander Y. Tsygankov" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/Alexander_Y_Tsygankov/"><strong>Alexander Y. Tsygankov</strong></a><br /> Department of Microbiology and Immunology<br /> <a href="https://www.omicsonline.org/universities/Temple_University/ ">Temple University School of Medicine</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Temple_University/" target="_blank" title="Temple University">Temple University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="I have been working in the area of signal transduction mediated by protein tyrosine phosphorylation for ~20 yr, publishing multiple papers on the functions of protein tyrosine kinases and their substrates. In particular, my laboratory has always been interested in the Cbl family. As a result of the interest in Cbl, we became co-discoverers of the TULA family; we identified and characterized TULA, a Cbl-associated protein. We then showed that TULA-2, but not TULA, is an active protein tyrosine phosphatase capable of dephosphorylating Syk. We later determined specificity of TULA-2, provided evidence that Syk is its bona-fide substrate, and characterized the overall effect of TULA-2-mediated dephosphorylation of Syk on GPVI signaling in platelets, a system that is uniquely convenient for studies of the role of TULA-2 in signaling regulation. My interests in platelet signaling and activation lead to establishing fruitful collaborations with several platelet experts working in Philadelphia, including Dr. Kunapuli of Temple University School of Medicine. This collaboration resulted in several publications focused on the functional role of TULA-2 in platelets. The current focus of these collaborative studies is on deciphering of molecular mechanisms of the down-regulatory function of TULA-2 in platelet signaling, both GPVI- and CLEC-2-mediated."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="My major interest lies in the area of cell signaling, in particular, of its regulation by protein tyrosine kinases and phosphatases. Previous work with protein kinases of Src and Syk families and adaptor proteins of Cbl family, which we among others demonstrated to be involved in Src- and Syk-mediated signaling, resulted in the discovery of the TULA family. We identified and characterized TULA, a Cbl-associated protein and later demonstrated that TULA-2, but not TULA, is an active protein tyrosine phosphatase capable of dephosphorylating Syk, which along with the highly-related kinase Zap-70 is a bona-fide substrate of TULA-2. Hence, my current interests are focused on understanding the role of TULA-family proteins in cell signaling and activation. This issue is addressed in two experimental systems – T lymphocytes and platelets. Our results indicate that TULA- and TULA-2-null mice are significantly more responsive to experimentally induced colitis and that this inflammation to a large degree depends on hyper-responsiveness of TULA-deficient T cells to stimulation through T-cell antigen receptor. These results are directly related to understanding of molecular and cellular mechanisms of inflammatory bowel disease. We have also shown that TULA-2-mediated dephosphorylation of Syk significantly reduces platelet signaling mediated by GPVI collagen receptor thus increasing the platelet activation threshold, which prevents unnecessary and potentially dangerous stimulation of platelet responses by sub-optimal stimuli. Our results indicate that TULA-2-null platelet exhibit greatly potentiated responses in vitro and in vivo. Likewise, pharmacological inhibition of TULA-2 by a novel compound appears to exert similar effects on platelets. Our current focus in these studies is deciphering the molecular mechanism of the down-regulatory function of TULA-2 in GPVI signaling and assessing the therapeutic potential of TULA-2 as a target in treatment of platelet-dependent bleeding disorders."> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_alexander_y_tsygankov.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-omid-akbari-19053.jpg" alt="Omid Akbari" title="Omid Akbari" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/Omid_Akbari/"><strong>Omid Akbari</strong></a><br /> Professor of Allergy and Immunology<br /> <a href="https://www.omicsonline.org/universities/University_of_Southern_California/ ">University of Southern California</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/University_of_Southern_California/" target="_blank" title="University of Southern California">University of Southern California</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="I have studied murine and human immune system for more than 20 years, and have made several key observations that have modified the prevailing disease paradigms (Please see science contribution section). I have a broad background in cellular and molecular Immunology, with specific training and expertise in key research areas such as innate and adaptive immune responses."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Allergy and Immunology"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_omid_akbari.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-alejandro-aballay-18924.jpg" alt="Alejandro Aballay" title="Alejandro Aballay" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/alejandro_aballay/"><strong>Alejandro Aballay</strong></a><br /> Department of Molecular Genetics and Microbiology<br /> <a href="https://www.omicsonline.org/universities/Duke_University/">Duke University Medical Center</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/Duke_University/" target="_blank" title="Duke University">Duke University</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Alejandro Aballay earned his bachelor’s degree in Pharmacy from Juan A. Maza University, in Mendoza, Argentina, in 1994. During this time, he worked as an undergraduate student at Nacional de Cuyo University, in Mendoza, Argentina, where he studied soil bioremediation. He finished his M.S. equivalent studies in 1995 and started exploring the machinery that governs early steps in endocytosis at Nacional de Cuyo University. During this period, he received a World Bank fellowship to complement his studies in endocytosis by working as a summer student for two consecutive years at Washington University, in St. Louis, Missouri. In 1998, he earned his Ph.D. at Nacional de Cuyo University and received a Pew Fellowship to move to St. Louis, where he continued his studies in endocytosis at Washington University. In 1999, following an interest in bacterial pathogenesis he developed while studying the intracellular transport of Brucella abortus when he was a graduate student, he moved to Boston to join the Ausubel laboratory at Harvard Medical School. Dr. Aballay moved to Durham in 2002 to join the Department of Molecular Genetics and Microbiology, where his studies focus on what makes bacteria pathogenic and hosts resistant. In the Ausubel laboratory, Dr. Aballay developed a novel pathogenesis system utilizing the simple well-studied nematode Caenorhabditis elegans and the common human bacterial pathogen Salmonella enterica. Salmonella is well known for its ability to cause food poisoning. Nematodes like C. elegans eat bacteria and surprisingly C. elegans is killed when it is provided S. enterica as a food source. This killing is accompanied by a persistent infection of S. enterica in the C. elegans intestine. Importantly, Dr. Aballay has shown that several well-studied S. enterica virulence factors required for causing disease in mammalian hosts are also required for C. elegans killing. This validates the use of C. elegans as a host to model Salmonella infection in mammals, including humans. Dr. Aballay’s laboratory takes advantage of the compromise between complexity and tractability of the C. elegans–S. enterica pathogenesis model. The focus of the laboratory is to use C. elegans as a host to screen thousands of bacterial clones from mutagenized libraries to identify novel Salmonella virulence factors and to address how they alter host signaling pathways. Since several components of innate immunity are conserved among different organisms throughout evolution, his group is also exploiting the genetic and genomic resources available for C. elegans to study the basis of the immune response. Dr. Aballay is a recipient of a number of awards, including: 2013 American Association for the Advancement of Science (AAAS) Fellow, 2009, Neuroimmunology of Brain Infections and Cancers Award, 2009 Howard Hughes Medical Institute (HHMI) Early Career Scientist Competition-Semifinalist, 2005 ICAAC Young Investigator Award, 2003 Whitehead Scholar in Biomedical Sciences, 1998 Pew Foundation Postdoctoral Fellowship."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Molecular Genetics and Microbiology, Immunology"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_alejandro_aballay.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-hong-zan-19047.jpg" alt="Hong Zan" title="Hong Zan" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/Hong_Zan/"><strong>Hong Zan</strong></a><br /> Department of Microbiology and Immunology <br /> School of Medicine<br /> <a href="https://www.omicsonline.org/universities/The_University_of_Texas/">The University of Texas Health Science Center</a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/the-university-of-texas/" target="_blank" title="The University of Texas">The University of Texas</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Hong Zan received his Ph.D. from Shanghai Institute of Biochemistry and Cell Biology (SIBCB), Chinese Academy of Sciences. He completed his Postdoc from Weill Medical College of Cornell University in 1999 and continued work in Weill Cornell Medical College until 2003. He moved to University of California, Irvine as a research scientist in the summer of 2003. In the end of 2013, Dr. Zan joined the faculty of the Department of Microbiology and Immunology in the School of Medicine at University of Texas Health Science Center, San Antonio, as an Associate Professor. Dr. Zan has extensive experience on immunology, Molecular Biology and autoimmunity. He has made significant contributions to the understanding of immunoglobulin class switch recombination and somatic hypermutation in antibody and autoantibody responses. He has published more than fifty papers, most of them are in high-profile journals, including Nature Immunology, Immunity, Cell Reports, Nature Struct. Mol. Biol., Nature Commun., Nature Rev. Immunol., EMBO J., J. Exp. Med., Trends Immunol. Dr. Zan serves as an Associate Editor of Autoimmunity since 2003. He is also editorial board member of eight other peer-reviewed scientific journals."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Dr. Zan has been working on B cell differentiation with emphasis on the molecular mechanisms of immunoglobulin gene expression, somatic hypermutation (SHM), class switch DNA recombination (CSR), memory B cell generation and maintenance, plasma cell differentiation, as well as antibody engineering, for over many years. He is also interested in the mechanism of antibody response to pathogenic antigens and autoantibody response in autoimmune diseases. He currently works on epigenetic regulation in antibody and autoantibody responses, and epigenetic modulators as therapeutics for autoimmune diseases, such as systemic lupus, and allergic diseases. Dr. Zan also interested in the tumoral genesis that related to dysregulation of SHM and CSR machinery. Expertise keywords: Immunology, Molecular Biology, B cell, Immunoglobulin, Epigenetics, DNA repair, Classs witching, Somatic hypermutation, Autoimmunity, Allergy"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_hong_zan.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-ghalib-alkhatib-19113.jpg" alt="Ghalib Alkhatib" title="Ghalib Alkhatib" class="img-responsive" width="85"> </td> <td align="left"> <p><a href="https://www.omicsonline.org/editor-profile/ghalib_alkhatib/"><strong>Ghalib Alkhatib</strong></a><br /> Virology/Bacteriology<br /> Drug Discovery Division<br /> Southern Research Institute<br /> USA</p> <p> </p> </td> <td align="center"> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Alkhatib obtained a Ph.D. in Molecular Virology from McGill University in Montreal, Canada in 1989. He completed his postdoctoral work at the Biotechnology Research Institute (BRI) in Montreal, where his research focused on the molecular immunology of natural killer (NK) cells. Subsequently, Dr. Alkhatib served as Visiting Fellow in the Laboratory of Viral Diseases at the National Institutes of Health in Bethesda, Maryland from 1995 to 1998. During his fellowship, he identified and characterized CCR5 as the coreceptor for the macrophage-tropic (M-tropic) HIV-1 isolates. As a result of this groundbreaking research, CCR5 is now the target for the development of drugs that block HIV-1 infection. Dr. Alkhatib has held several academic positions, including Assistant Professor in the Department of Microbiology and Immunology at the Indiana University School of Medicine in Indianapolis from 1997 to 2002 and Associate Professor in the Department of Microbiology and Immunology at the Indiana University School of Medicine from 2003 to 2010. Dr. Alkhatib joined Southern Research Institute in July 2012, having previously served since 2010 as Professor in the Department of Biomedical Sciences and Center of Excellence for Infectious Diseases in the Paul L. Foster School of Medicine at Texas Tech University Health Sciences Center in El Paso, Texas."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Dr. Alkhatib’s research is focused on understanding how interaction of HIV-1 (AIDS virus) and HTLV-1 (human T cell leukemia virus) envelope glycoproteins with host cell receptors lead to membrane fusion and viral entry. Analyzing the mechanisms of retroviral entry is a key step in the development of anti-viral agents. Specifically, Dr. Alkhatib’s research focuses on the mechanisms of genetic resistance to HIV-1 infection. HIV-1 requires CD4 and a coreceptor (CCR5 or CXCR4) for entry into susceptible host cells. CCR5 and CXR4 belong to the family of seven transmembrane spanner proteins. A naturally occurring frame-shift mutation caused by a 32 base-pair deletion (Δ32) in the human CCR5 gene is highly associated with protection against HIV-1. CCR5Δ32 is a loss-of-function mutation that abolishes cell surface expression of the HIV coreceptor CCR5 and provides resistance to HIV-1 infection. Published work from Dr. Alkhatib’s laboratory suggest that at least two distinct mechanisms may account for genetic resistance to HIV-1 conferred by CCR5Δ32: loss of wild type CCR5 surface expression and generation of CCR5Δ32 truncated protein, which functions as a scavenger of both CCR5 and CXCR4. Understanding how CCR5Δ32 interacts with the HIV coreceptors will lead to novel findings concerning coreceptor structure-function that may be utilized for the design of drugs that mimic the CCR5Δ32 activity. Dr. Alkhatib’s laboratory is actively pursuing the expression and purification of sufficient quantities of CCR5 protein for studying its crystal structure. Since the discovery of CCR5 as a HIV coreceptor, efforts to express large quantities of CCR5 have promising. The crystal structures of CCR5-bound chemokine or gp120 are not yet resolved. This can be a great project for hard working graduate students. Members in the laboratory are currently examining a number of CCR5 mutants to analyze structure/function relationship of this extraordinary HIV coreceptor. Our long term goal is to map the critical determinants of CCR5 involved in HIV-1 entry into the target cells (please see attached video clip). During the course of analysis of genetic resistance to HIV members of the lab isolated unique HIV-1 envelope glycoproteins from infected individuals that are homozygous for the CCR5Δ32 mutation. We consider these envelopes as unique because they were cloned from viruses that replicated in CCR5-deficient cells/individuals. Sequence analysis of these unique envelope glycoproteins indicated unique polymorphisms in gp120 and gp41 that might account for the functional differences in their fusion activities. Current projects in the lab focus on these functional differences. Other areas of interest in Dr. Akhatib’s laboratory include the mechanism of viral entry by the human T cell leukemia virus type 1 (HTLV-1). Our long term goal is to determine the mechanism of preferential tropism of HTLV-1 to CD4+ T lymphocytes in vivo. It has previously been determined that the erythrocyte glucose transporter protein (GLUT-1) is a cellular receptor for HTLV-1. GLUT-1 is expressed in almost all cell types and did explain HTLV-1 preferential tropism to CD4+ T cells in vivo, however, it could represent one component of the HTLV-1 receptor complex. The GLUT-1 receptor is a multi-spanner membrane protein that crosses the plasma membrane 12 times. The common use by HIV-1 and HTLV-1 of these multi-spanning membrane proteins may lead to the identification of common retroviral entry mechanisms and may lead to design of drugs that inhibit retroviral entry."> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_ghalib_alkhatib.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-eduardo-seclen-hidalgo-19638.jpg" alt="Eduardo Seclen Hidalgo" title="Eduardo Seclen Hidalgo" class="img-responsive" width="85"> </td> <td align="left"> <p><strong><a href="https://www.omicsonline.org/editor-profile/eduardo_seclen_hidalgo/">Eduardo Seclen Hidalgo</a> </strong><br /> Molecular Microbiology and Immunology<br /> <a href="https://www.omicsonline.org/universities/University_of_Southern_California/">Univ. of Southern California </a><br /> USA</p> </td> <td align="center"> <a href="https://www.omicsonline.org/universities/University_of_Southern_California/" target="_blank" title="University of Southern California">University of Southern California</a> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Eduardo Seclen Hidalgo a Research Associate at the University of Southern California, where he works in in hematopoietic stem cells focused on HIV research. He obtained his PhD from the University of Complutense in Madrid, Spain studying ways to characterize HIV viral tropism, and its impact in the pathogenesis of the infection and response to antiretroviral treatment. In the last 3 years, his research have been enriched by his participation in projects using gene therapy in hematopoietic stem cells as an approach to fight genetic and infectious diseases, including HIV. His research have been funded by prestigious fellowships provided by the AIDS foundation “Fundación de Investigación y Prevención del SIDA en España”, the National Health Institution “Instituto de Salud Carlos III” and, more recently, the “California Institute for Regenerative Medicine”."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="HIV virology HIV tropism HIV pathogenesis Antiretroviral treatment, especially entry inhibitors Bone marrow transplantation as approach to fight HIV Gene therapy in stem cells as approach to fight infectious diseases, including HIV HIV latency, especially use of vectors to disrupt latency in vivo and mouse models"> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_eduardo_seclen_hidalgo.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> <tr> <td align="center" width="15%"> <img src="https://www.omicsgroup.org/articles-admin/photos/journalofmolecularimmunology-bozena-futoma-koloch-19639.jpg" alt="Bozena Futoma Koloch" title="Bozena Futoma Koloch" class="img-responsive" width="85"> </td> <td align="left"> <p><strong><a href="https://www.omicsonline.org/editor-profile/bozena_futoma_koloch/">Bozena Futoma Koloch</a> </strong><br /> Institute of Genetics and Microbiology <br /> University of Wroclaw <br /> Poland</p> </td> <td align="center"> </td> <td align="left" width="22%"> <div class="list-group list-group-flush m-b-0 a-pointer"> <a tabindex="0" class="list-group-item list-group-item-action text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Biography" data-placement="left" data-content="Dr. Bo脜录ena Futoma-Ko脜鈥歰ch graduated from University of Wroc脜鈥歛w in 2004. She received her PhD mentored by Prof. W. Doroszkiewicz in microbiology from the University of Wroc脜鈥歛w in 2008. After that she has held academic position of Assistant Professor in the Department of Microbiology in the Institute of Genetics and Microbiology at University of Wroc脜鈥歛w. She is a member of Polish Society of Microbiologists (which belongs to the Federation of European Microbiological Societies - FEMS), European Society of Clinical Microbiology and Infectious Diseases - ESCMID, and International Complement Society - ICS. She has published more than 50 papers in national and international journals, 30 presentations at congresses, with several awards. Dr. Futoma-Ko脜鈥歰ch's research program focuses on the bacterial surface antigens: lipopolysaccharide (LPS, endotoxin) and outer membrane proteins (OMP) as molecular targets of the protective immune response against pathogenic bacteria, especially Salmonella. Investigations on susceptibility of Salmonella strains possessing sialic acid-containing LPS to human serum (HS) resulted in many publications about the role of atypical bacterial endotoxin in determining complement system activation through the alternative pathway. It was also shown that differential sensitivity of tested bacteria to HS might be due to a weaker C3 serum protein activation on strongly sialylated LPS and a binding of C3 components to the OMP."> Biography </a> <a tabindex="0" class="list-group-item text-warning" role="button" data-html="true" data-container="body" data-toggle="popover" data-trigger="focus" title="Research Interest" data-placement="left" data-content="Investigations of surface molecular targets of the protective immune response against pathogenic bacteria. Participation of lipopolysaccharide and outer membrane proteins in determining bacterial susceptibility to serum complement-mediated killing."> Research Interest </a> <a href="https://www.omicsonline.org/download.php?download=JMIimages/certificate_bozena_futoma_koloch.jpg" title="Click here" class="list-group-item text-warning">Network</a> </div> </td> </tr> </table> </div> </div> </div> </div> </div> </div> </div> </div>  <div class="container"> <div class="row"> <div class="col"> <div class="bg-white shadow-3dp px-3"> <div class="row"> </div> <div class="row my-3"> <div class="col-12"> <h6 class="text-warning font-weight-600">Peer Reviewed Journals</h6> <p><strong>Make the best use of Scientific Research and information from our 700 + peer reviewed, <a href="https://www.omicsonline.org/open-access-journals-list.php" title="Click here">Open Access Journals</a></strong> </p> </div> </div> <div class="row">  <div class="col-md-6"> <div class="card border-orange-800"> <h3 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Editorial Board Members - Journal of Molecular Immunology