TIM-3 drives temporal differences in restimulation-induced cell death sensitivity in effector CD8⁺ T cells in conjunction with CEACAM1.

ABSTRACT: Immune homeostasis depends upon effective clearance of pathogens while simultaneously preventing autoimmunity and immunopathology in the host. Restimulation-induced cell death (RICD) is one such mechanism where by activated T cells receive subsequent antigenic stimulation, reach a critical signal threshold through the T cell receptor (TCR), and commit to apoptosis. Many details of this process remain unclear, including the role of co-stimulatory and co-inhibitory proteins that influence the TCR signaling cascade. Here we characterize the role of T cell immunoglobulin and mucin domain containing 3 (TIM-3) in RICD regulation. TIM-3 protected newly activated CD8⁺ effector T cells from premature RICD during clonal expansion. Surprisingly, however, we found that TIM-3 potentiated RIC

SUBMITTER: Lake CM 

PROVIDER: S-EPMC8046753 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature