TY - JOUR
T1 - Receptor transfer between immune cells by autoantibody-enhanced, CD32-driven trogocytosis is hijacked by HIV-1 to infect resting CD4 T cells
AU - Albanese, Manuel
AU - Chen, Hong Ru
AU - Gapp, Madeleine
AU - Muenchhoff, Maximilian
AU - Yang, Hsiu Hui
AU - Peterhoff, David
AU - Hoffmann, Katja
AU - Xiao, Qianhao
AU - Ruhle, Adrian
AU - Ambiel, Ina
AU - Schneider, Stephanie
AU - Mejías-Pérez, Ernesto
AU - Stern, Marcel
AU - Wratil, Paul R.
AU - Hofmann, Katharina
AU - Amann, Laura
AU - Jocham, Linda
AU - Fuchs, Thimo
AU - Ulivi, Alessandro F.
AU - Besson-Girard, Simon
AU - Weidlich, Simon
AU - Schneider, Jochen
AU - Spinner, Christoph D.
AU - Sutter, Kathrin
AU - Dittmer, Ulf
AU - Humpe, Andreas
AU - Baumeister, Philipp
AU - Wieser, Andreas
AU - Rothenfusser, Simon
AU - Bogner, Johannes
AU - Roider, Julia
AU - Knolle, Percy
AU - Hengel, Hartmut
AU - Wagner, Ralf
AU - Laketa, Vibor
AU - Fackler, Oliver T.
AU - Keppler, Oliver T.
N1 - Publisher Copyright:
© 2024 The Authors
PY - 2024/4/16
Y1 - 2024/4/16
N2 - 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.
AB - 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.
KW - CD32
KW - CRISPR-Cas9
KW - HIV reservoir
KW - autoantibodies
KW - immune cell communication
KW - trogocytosis
UR - http://www.scopus.com/inward/record.url?scp=85189971046&partnerID=8YFLogxK
U2 - 10.1016/j.xcrm.2024.101483
DO - 10.1016/j.xcrm.2024.101483
M3 - Article
C2 - 38579727
AN - SCOPUS:85189971046
SN - 2666-3791
VL - 5
JO - Cell Reports Medicine
JF - Cell Reports Medicine
IS - 4
M1 - 101483
ER -
