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Albanese, M.* ; Chen, H.R.* ; Gapp, M.* ; Muenchhoff, M.* ; Yang, H.H.* ; Peterhoff, D.* ; Hoffmann, K.* ; Xiao, Q.* ; Ruhle, A.* ; Ambiel, I.* ; Schneider, S.* ; Mejias-Perez, E.* ; Stern, M.* ; Wratil, P.R.* ; Hofmann, K.* ; Amann, L.* ; Jocham, L.* ; Fuchs, T.* ; Ulivi, A.F.* ; Besson-Girard, S.* ; Weidlich, S.* ; Schneider, J.* ; Spinner, C.D.* ; Sutter, K.* ; Dittmer, U.* ; Humpe, A.* ; Baumeister, P.* ; Wieser, A.* ; Rothenfußer, S. ; Bogner, J.* ; Roider, J.* ; Knolle, P.* ; Hengel, H.* ; Wagner, R.* ; Laketa, V.* ; Fackler, O.T.* ; Keppler, O.T.*

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

Cell Rep. Med. 5:101483 (2024)

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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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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Cd32 ; Crispr-cas9 ; Hiv Reservoir ; Autoantibodies ; Immune Cell Communication ; Trogocytosis; Fc-gamma-receptor; Dendritic Cells; Dc-sign; Antibody; Molecules; Acquisition; Activation; Expression; Neutralization; Involvement

ISSN (print) / ISBN 2666-3791

e-ISSN 2666-3791

Journal Cell Reports Medicine

Quellenangaben Volume: 5, Issue: 4, Article Number: 101483

Publisher Cell Press

Publishing Place 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Unit for Clinical Pharmacology (KKG-EKLiP)

Grants Deutsche Zentrum fur Infektionsforschung (DZIF)
Clinical leave fellowship
China Scholarship Council: Fellowship
LMUexcellent: LMU Research Fellowship
Friedrich-Baur-Foundation: Young scientist grant

Deutsche Forschungsgemeinschaft