ORCID: https://orcid.org/0000-0002-4614-7599; Chen, Hong-Ru; Gapp, Madeleine; Muenchhoff, Maximilian ORCID: https://orcid.org/0000-0001-7016-0470; Yang, Hsiu-Hui; Peterhoff, David; Hoffmann, Katja; Xiao, Qianhao; Ruhle, Adrian ORCID: https://orcid.org/0000-0002-8132-9814; Ambiel, Ina; Schneider, Stephanie; Mejías-Pérez, Ernesto; Stern, Marcel; Wratil, Paul R.; Hofmann, Katharina; Amann, Laura; Jocham, Linda; Fuchs, Thimo; Ulivi, Alessandro F.; Besson-Girard, Simon; Weidlich, Simon; Schneider, Jochen; Spinner, Christoph D.; Sutter, Kathrin; Dittmer, Ulf; Humpe, Andreas; Baumeister, Philipp; Wieser, Andreas; Rothenfusser, Simon ORCID: https://orcid.org/0000-0003-1151-7614; Bogner, Johannes R. ORCID: https://orcid.org/0000-0001-8628-1533; Roider, Julia ORCID: https://orcid.org/0000-0002-1347-2838; Knolle, Percy; Hengel, Hartmut; Wagner, Ralf; Laketa, Vibor; Fackler, Oliver T. und Keppler, Oliver Till ORCID: https://orcid.org/0000-0002-1384-8946
(2024):
Receptor transfer between immune cells by autoantibody-enhanced, CD32-driven trogocytosis is hijacked by HIV-1 to infect resting CD4 T cells.
In: Cell Reports Medicine, Bd. 5, Nr. 4, 101483
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Abstract
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.
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