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

Albanese, Manuel and Chen, Hong-Ru and Gapp, Madeleine and Muenchhoff, Maximilian and Yang, Hsiu-Hui and Peterhoff, David and Hoffmann, Katja and Xiao, Qianhao and Ruhle, Adrian and Ambiel, Ina and Schneider, Stephanie and Mejias-Perez, Ernesto and Stern, Marcel and Wratil, Paul R. and Hofmann, Katharina and Amann, Laura and Jocham, Linda and Fuchs, Thimo and Ulivi, Alessandro F. and Besson-Girard, Simon and Weidlich, Simon and Schneider, Jochen and Spinner, Christoph D. and Sutter, Kathrin and Dittmer, Ulf and Humpe, Andreas and Baumeister, Philipp and Wieser, Andreas and Rothenfusser, Simon and Bogner, Johannes and Roider, Julia and Knolle, Percy and Hengel, Hartmut and Wagner, Ralf and Laketa, Vibor and Fackler, Oliver T. and Keppler, Oliver T. (2024) Receptor transfer between immune cells by autoantibody-enhanced, CD32-driven trogocytosis is hijacked by HIV-1 to infect resting CD4 T cells. CELL REPORTS MEDICINE, 5 (4): 101483. ISSN 2666-3791,

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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 Fcy 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.

Item Type: Article
Uncontrolled Keywords: FC-GAMMA-RECEPTOR; DENDRITIC CELLS; DC-SIGN; ANTIBODY; MOLECULES; ACQUISITION; EXPRESSION; NEUTRALIZATION; INVOLVEMENT; LYMPHOCYTES;
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Medizinische Mikrobiologie und Hygiene
Depositing User: Dr. Gernot Deinzer
Date Deposited: 06 Aug 2025 06:51
Last Modified: 06 Aug 2025 06:51
URI: https://pred.uni-regensburg.de/id/eprint/65681

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