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

MPG-Autoren
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Ulivi,  Alessandro F.
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Albanese, M., Chen, H.-R., Gapp, M., Muenchhoff, M., Yang, H.-H., Peterhoff, D., et al. (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. doi:10.1016/j.xcrm.2024.101483.


Zitierlink: https://hdl.handle.net/21.11116/0000-000F-7C03-3
Zusammenfassung
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.