دورية أكاديمية
أعرض في EDS

Receptor transfer between immune cells by autoantibody-enhanced, CD32-driven trogocytosis is hijacked by HIV-1 to infect resting CD4 T cells.

التفاصيل البيبلوغرافية
العنوان: Receptor transfer between immune cells by autoantibody-enhanced, CD32-driven trogocytosis is hijacked by HIV-1 to infect resting CD4 T cells.
المؤلفون: Albanese M; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany; Department for Clinical Sciences and Community Health (DISCCO), University of Milan, Milan, Italy., Chen HR; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany. Electronic address: hong-ru@besson-girard.fr., Gapp M; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Muenchhoff M; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany., Yang HH; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Peterhoff D; Institute of Medical Microbiology and Hygiene, Molecular Microbiology (Virology), University of Regensburg, Regensburg, Germany., Hoffmann K; Institute of Virology, University Medical Center, Albert-Ludwigs-University Freiburg, Freiburg, Germany., Xiao Q; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Ruhle A; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Ambiel I; Department of Infectious Diseases, Heidelberg University, Medical Faculty Heidelberg, Integrative Virology, Center for Integrative Infectious Disease Research (CIID), Heidelberg, Germany; German Centre for Infection Research (DZIF), Partner Site Heidelberg, Heidelberg, Germany., Schneider S; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Mejías-Pérez E; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Stern M; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Wratil PR; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Hofmann K; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Amann L; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Jocham L; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Fuchs T; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany., Ulivi AF; Max Planck Institute of Psychiatry, Munich, Germany., Besson-Girard S; Institute for Stroke and Dementia Research, University Hospital, LMU München, Munich, Germany., Weidlich S; Technical University of Munich, School of Medicine, University Hospital Rechts der Isar, Department of Internal Medicine II, Munich, Germany., Schneider J; Technical University of Munich, School of Medicine, University Hospital Rechts der Isar, Department of Internal Medicine II, Munich, Germany., Spinner CD; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany; Technical University of Munich, School of Medicine, University Hospital Rechts der Isar, Department of Internal Medicine II, Munich, Germany., Sutter K; University Hospital Essen, University Duisburg-Essen, Institute for Virology and Institute for Translational HIV Research, Essen, Germany., Dittmer U; University Hospital Essen, University Duisburg-Essen, Institute for Virology and Institute for Translational HIV Research, Essen, Germany., Humpe A; Department of Transfusion Medicine, Cell Therapeutics, and Hemostaseology, Department of Anesthesiology, University Hospital Munich, Munich, Germany., Baumeister P; Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital, LMU München, Munich, Germany., Wieser A; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany; Max von Pettenkofer Institute, Medical Microbiology and Hospital Epidemiology, Faculty of Medicine, LMU München, Munich, Germany; Division of Infectious Diseases and Tropical Medicine, University Hospital, LMU München, Munich, Germany., Rothenfusser S; Division of Clinical Pharmacology, University Hospital, LMU München and Unit Clinical Pharmacology (EKliP), Helmholtz Center for Environmental Health, Munich, Germany., Bogner J; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany; Division of Infectious Diseases, University Hospital, Medizinische Klinik und Poliklinik IV, LMU München, Munich, Germany., Roider J; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany; Division of Infectious Diseases, University Hospital, Medizinische Klinik und Poliklinik IV, LMU München, Munich, Germany., Knolle P; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany; Institute of Molecular Immunology and Experimental Oncology, School of Medicine, Technical University of Munich (TUM), Munich, Germany., Hengel H; Institute of Virology, University Medical Center, Albert-Ludwigs-University Freiburg, Freiburg, Germany., Wagner R; Institute of Medical Microbiology and Hygiene, Molecular Microbiology (Virology), University of Regensburg, Regensburg, Germany., Laketa V; German Centre for Infection Research (DZIF), Partner Site Heidelberg, Heidelberg, Germany; Department of Infectious Diseases, Heidelberg University, Medical Faculty Heidelberg, Virology, Center for Integrative Infectious Disease Research (CIID), Heidelberg, Germany., Fackler OT; Department of Infectious Diseases, Heidelberg University, Medical Faculty Heidelberg, Integrative Virology, Center for Integrative Infectious Disease Research (CIID), Heidelberg, Germany; German Centre for Infection Research (DZIF), Partner Site Heidelberg, Heidelberg, Germany. Electronic address: oliver.fackler@med.uni-heidelberg.de., Keppler OT; Max von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU München, Munich, Germany; German Centre for Infection Research (DZIF), Partner Site Munich, Munich, Germany. Electronic address: keppler@mvp.lmu.de.
المصدر: Cell reports. Medicine [Cell Rep Med] 2024 Apr 16; Vol. 5 (4), pp. 101483. Date of Electronic Publication: 2024 Apr 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101766894 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2666-3791 (Electronic) Linking ISSN: 26663791 NLM ISO Abbreviation: Cell Rep Med Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2020]-
مواضيع طبية MeSH: HIV-1* , HIV Infections* , HIV Seropositivity*, Humans ; CD4-Positive T-Lymphocytes ; Receptors, IgG/metabolism ; Autoantibodies/metabolism ; Trogocytosis
مستخلص: Immune cell phenotyping frequently detects lineage-unrelated receptors. Here, we report that surface receptors can be transferred from primary macrophages to CD4 T cells and identify the Fcγ receptor CD32 as driver and cargo of this trogocytotic transfer. Filamentous CD32 + nanoprotrusions deposit distinct plasma membrane patches onto target T cells. Transferred receptors confer cell migration and adhesion properties, and macrophage-derived membrane patches render resting CD4 T cells susceptible to infection by serving as hotspots for HIV-1 binding. Antibodies that recognize T cell epitopes enhance CD32-mediated trogocytosis. Such autoreactive anti-HIV-1 envelope antibodies can be found in the blood of HIV-1 patients and, consistently, the percentage of CD32 + CD4 T cells is increased in their blood. This CD32-mediated, antigen-independent cell communication mode transiently expands the receptor repertoire and functionality of immune cells. HIV-1 hijacks this mechanism by triggering the generation of trogocytosis-promoting autoantibodies to gain access to immune cells critical to its persistence.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
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فهرسة مساهمة: Keywords: CD32; CRISPR-Cas9; HIV reservoir; autoantibodies; immune cell communication; trogocytosis
المشرفين على المادة: 0 (Receptors, IgG)
0 (Autoantibodies)
تواريخ الأحداث: Date Created: 20240405 Date Completed: 20240419 Latest Revision: 20240426
رمز التحديث: 20240426
مُعرف محوري في PubMed: PMC11031382
DOI: 10.1016/j.xcrm.2024.101483
PMID: 38579727
قاعدة البيانات: MEDLINE
الوصف
تدمد:2666-3791
DOI:10.1016/j.xcrm.2024.101483