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<!doctype html> <html lang="de"> <head> <title>Charakterisierung in vitro erzeugter menschlicher polarisier | 50614</title> <meta name="keywords" content="Salma Iqbal und Ashok Kumar , "/> <meta name="description" content="Ziel: Der Kontakt mit eindringenden Krankheitserregern und/oder Gewebeverletzungen führt zur Polarisierung von Makrophagen in einen M1- oder M2-Zustan..50614"/> <meta name="citation_publisher" content="Longdom Publishing SL" /> <meta name="citation_journal_title" content="Zeitschrift für klinische und zelluläre Immunologie"> <meta name="citation_title" content="Charakterisierung in vitro erzeugter menschlicher polarisierter Makrophagen "> <meta name="citation_author" content="Salma Iqbal und Ashok Kumar" /> <meta name="citation_year" content=""> <meta name="citation_volume" content="6"> <meta name="citation_issue" content="6"> <meta name="citation_abstract" content="Ziel: Der Kontakt mit eindringenden Krankheitserregern und/oder Gewebeverletzungen führt zur Polarisierung von Makrophagen in einen M1- oder M2-Zustand, der weiter in die Untergruppen M2a, M2b und M2c unterteilt wird. Die menschlichen Makrophagen-Untergruppen sind bisher nur unzureichend charakterisiert. Die vorliegende Studie wurde durchgeführt, um die Makrophagenpolarisierung anhand einer nicht abschließenden Reihe von Oberflächenmarkern in Bezug auf M1-, M2a-, M2b- und M2c-Makrophagen und die Produktion von entzündungsfördernden und entzündungshemmenden Zytokinen als Reaktion auf verschiedene Toll-like-Rezeptoren (TLR)-Liganden zu charakterisieren. Methoden: Wir haben verschiedene Makrophagen-Subtypen erzeugt, indem wir aus Monozyten stammende Makrophagen (MDMs) mit IFNγ (M1), IL-4 (M2a), LPS und IL-1β (M2b) oder IL-10 (M2c) behandelt und anschließend mit Toll-like-Rezeptor (TLR)-2-, TLR-3- und TLR-4-Agonisten stimuliert haben. Die Analyse der Expression von Oberflächenmarkern und Zytokinen wurde per Durchflusszytometrie bzw. ELISA durchgeführt. Ergebnisse: Die M2a-Subgruppe war durch den Phänotyp CD14 niedrig , CD163 niedrig und TLR4 niedrig gekennzeichnet und produzierte hohe IL-10-Werte. Die M2b-Subgruppe war durch den Phänotyp CD14 hoch , CD80 hoch und CD200R niedrig gekennzeichnet und produzierte vor der Stimulation IL-6. Die M2c-Subgruppe zeigte einen Phänotyp CD86 niedrig , CD163 hoch und produzierte hohe IL-10-Werte. Die M1-Untergruppe war durch den Phänotyp CD80 hoch , CD86 hoch , CD163 niedrig und TLR4 hoch gekennzeichnet und produzierte nach Stimulation hohe Konzentrationen von proinflammatorischem IFN-g, IL-12, TNFα und IL-23. Schlussfolgerung: Diese Studie charakterisiert alle vier Polarisationszustände in menschlichen Makrophagen. Jeder Polarisationszustand zeigte ein einzigartiges Zelloberflächenmarkerprofil und Zytokinprofil. Diese phänotypischen Marker können verwendet werden, um Makrophagenpopulationen bei entzündlichen Gewebeerkrankungen in vivo zu charakterisieren und so die Krankheitspathogenese besser zu verstehen. 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title="Hier klicken">Pharmazeutische Wissenschaften</a><br> <a class="nav-item nav-link" href="https://german.longdom.org/business-and-management-journals.html" title="Hier klicken">Wirtschaft & Management</a><br> </nav> </div> </div>  </aside> <div class="col-12 col-sm-9"> <h2 class="heading-1">Abstrakt</h2> <h3 class="">Charakterisierung in vitro erzeugter menschlicher polarisierter Makrophagen </h3> <p> <i class="fas fa-user"></i> Salma Iqbal und Ashok Kumar </p> <p><strong>Ziel:</strong> Der Kontakt mit eindringenden Krankheitserregern und/oder Gewebeverletzungen führt zur Polarisierung von Makrophagen in einen M1- oder M2-Zustand, der weiter in die Untergruppen M2a, M2b und M2c unterteilt wird. Die menschlichen Makrophagen-Untergruppen sind bisher nur unzureichend charakterisiert. Die vorliegende Studie wurde durchgeführt, um die Makrophagenpolarisierung anhand einer nicht abschließenden Reihe von Oberflächenmarkern in Bezug auf M1-, M2a-, M2b- und M2c-Makrophagen und die Produktion von entzündungsfördernden und entzündungshemmenden Zytokinen als Reaktion auf verschiedene Toll-like-Rezeptoren (TLR)-Liganden zu charakterisieren. <br /> <strong>Methoden:</strong> Wir haben verschiedene Makrophagen-Subtypen erzeugt, indem wir aus Monozyten stammende Makrophagen (MDMs) mit IFNγ (M1), IL-4 (M2a), LPS und IL-1β (M2b) oder IL-10 (M2c) behandelt und anschließend mit Toll-like-Rezeptor (TLR)-2-, TLR-3- und TLR-4-Agonisten stimuliert haben. Die Analyse der Expression von Oberflächenmarkern und Zytokinen wurde per Durchflusszytometrie bzw. ELISA durchgeführt. <br /> <strong>Ergebnisse: Die M2a-Subgruppe war durch den Phänotyp CD14 </strong><sup>niedrig</sup> , CD163 <sup>niedrig</sup> und TLR4 <sup>niedrig</sup> gekennzeichnet und produzierte hohe IL-10-Werte. Die M2b-Subgruppe war durch den Phänotyp CD14 <sup>hoch</sup> , CD80 <sup>hoch</sup> und CD200R <sup>niedrig</sup> gekennzeichnet und produzierte vor der Stimulation IL-6. Die M2c-Subgruppe zeigte einen Phänotyp CD86 <sup>niedrig</sup> , CD163 <sup>hoch</sup> und produzierte hohe IL-10-Werte. Die M1-Untergruppe war durch den Phänotyp CD80 <sup>hoch</sup> , CD86 <sup>hoch</sup> , CD163 <sup>niedrig</sup> und TLR4 <sup>hoch</sup> gekennzeichnet und produzierte nach Stimulation hohe Konzentrationen von proinflammatorischem IFN-g, IL-12, TNFα und IL-23. <br /> <strong>Schlussfolgerung:</strong> Diese Studie charakterisiert alle vier Polarisationszustände in menschlichen Makrophagen. Jeder Polarisationszustand zeigte ein einzigartiges Zelloberflächenmarkerprofil und Zytokinprofil. Diese phänotypischen Marker können verwendet werden, um Makrophagenpopulationen bei entzündlichen Gewebeerkrankungen in vivo zu charakterisieren und so die Krankheitspathogenese besser zu verstehen.</p> <div class="alert alert-info text-left"><b>Haftungsausschluss:</b> Diese Zusammenfassung wurde mithilfe von Tools der k眉nstlichen Intelligenz 眉bersetzt und wurde noch nicht 眉berpr眉ft oder verifiziert.</div> <div class="nav social-icons"> <a class="nav-link w-auto">Teile diesen Artikel</a> <a title="Hier klicken" target="_blank" href="https://www.facebook.com/sharer.php?u=https://german.longdom.org/abstract/characterization-of-emin-vitroem-generated-human-polarized-macrophages-50614.html" rel="noopener"><i class="fab fa-facebook-f"></i></a> <a class="nav-link" title="Hier klicken" target="_blank" href="https://twitter.com/share?url=https://german.longdom.org/abstract/characterization-of-emin-vitroem-generated-human-polarized-macrophages-50614.html" rel="noopener"><i class="fab fa-twitter"></i></a> <a class="nav-link" title="Hier klicken" target="_blank" href="https://www.linkedin.com/shareArticle?mini=true&url=https://german.longdom.org/abstract/characterization-of-emin-vitroem-generated-human-polarized-macrophages-50614.html" rel="noopener"><i class="fab fa-linkedin-in"></i></a> <a class="nav-link" title="Hier klicken" target="_blank" href="https://plus.google.com/share?url=https://german.longdom.org/abstract/characterization-of-emin-vitroem-generated-human-polarized-macrophages-50614.html" rel="noopener"><i class="fab fa-google-plus-g"></i></a> </div> </div> </div> </div> </section> <footer class="bg-blue-grey-900 py-3"> <div class="container"> <div class="row"> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Inhaltslinks</h4> <ul class="list-unstyled footer-links font-size-3"> <li><a class="" href="https://german.longdom.org/privacy-policy.html" title="Hier klicken">Datenschutzrichtlinie</a></li> <li><a class="" href="https://german.longdom.org/terms-conditions.html" title="Hier klicken">Allgemeine Gesch盲ftsbedingungen</a></li> <li><a class="" href="https://german.longdom.org/authors-reviewers-editors.html" title="Hier klicken">Autoren, Gutachter & Herausgeber</a></li> </ul> </div> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Kontaktieren Sie Longdom</h4> <p><strong>Longdom Group SA</strong><br /> Avenue Roger Vandendriessche,<br /> 18, 1150 Br眉ssel, Belgien<br /> Telefon: +442038085340<br /> <strong>E-Mail:</strong> <a class="white" href="mailto:info@longdom.org" title="Hier klicken">info@longdom.org</a></p> </div> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Verbinden</h4> <nav class="nav nav-pills social-icons-footer flex-column a-pl-0"> <a href="https://www.facebook.com/longdompublisher" title="Hier klicken" target="_blank" class="nav-link bg-facebook-hover"><i class="fab fa-facebook-f bg-facebook"></i></a> <a href="https://www.linkedin.com/company/longdom-publishing-sl/" title="Hier klicken" target="_blank" class="nav-link bg-linkedin-hover"><i class="fab fa-linkedin-in bg-linkedin"></i></a> <a href="https://twitter.com/LongdomP" title="Hier klicken" target="_blank" class="nav-link bg-twitter-hover"><i class="fab fa-twitter bg-twitter"></i></a> <a href="https://www.instagram.com/longdom_publisher/" title="Hier klicken" target="_blank" class="nav-link bg-instagram-hover"><i class="fab fa-instagram bg-instagram"></i></a> </nav> </div> </div> <div class="row text-center"> <div class="col"> <p>Urheberrechte 漏 © 2025 <a href="https://german.longdom.org/" title="Hier klicken" class="white">Longdom Publishing SL</a>.</p> </div> </div> </div> </footer>  <a href="#0" class="cd-top js-cd-top">Top</a>   <script src="https://code.jquery.com/jquery-3.3.1.min.js"></script> <script src="https://cdnjs.cloudflare.com/ajax/libs/popper.js/1.14.7/umd/popper.min.js"></script> <script src="https://stackpath.bootstrapcdn.com/bootstrap/4.3.1/js/bootstrap.min.js"></script>  <script> jQuery(function($) { $(window).scroll(function fix_element() { $('#target').css( $(window).scrollTop() > 100 ? 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