Signaling through the Inhibitory Fc Receptor FcγRIIB Induces CD8⁺ T Cell Apoptosis to Limit T Cell Immunity.

ABSTRACT: Effector CD8⁺ T cells are important mediators of adaptive immunity, and receptor-ligand interactions that regulate their survival may have therapeutic potential. Here, we identified a subset of effector CD8⁺ T cells that expressed the inhibitory fragment crystallizable (Fc) receptor FcγRIIB following activation and multiple rounds of division. CD8⁺ T cell-intrinsic genetic deletion of Fcgr2b increased CD8⁺ effector T cell accumulation, resulting in accelerated graft rejection and decreased tumor volume in mouse models. Immunoglobulin G (IgG) antibody was not required for FcγRIIB-mediated control of CD8⁺ T cell immunity, and instead, the immunosuppressive cytokine fibrinogen-like 2 (Fgl2) was a functional ligand for FcγRIIB on CD8⁺

SUBMITTER: Morris AB 

PROVIDER: S-EPMC7326381 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature