English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

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

MPS-Authors
/persons/resource/persons262526

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

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: https://hdl.handle.net/21.11116/0000-000F-7C03-3
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.