Checkpoint Receptor TIGIT Expressed on Tim-1⁺ B Cells Regulates Tissue Inflammation.

ABSTRACT: Tim-1, a phosphatidylserine receptor expressed on B cells, induces interleukin 10 (IL-10) production by sensing apoptotic cells. Here we show that mice with B cell-specific Tim-1 deletion develop tissue inflammation in multiple organs including spontaneous paralysis with inflammation in the central nervous system (CNS). Transcriptomic analysis demonstrates that besides IL-10, Tim-1⁺ B cells also differentially express a number of co-inhibitory checkpoint receptors including TIGIT. Mice with B cell-specific TIGIT deletion develop spontaneous paralysis with CNS inflammation, but with limited inflammation in other organs. Our findings suggest that Tim-1⁺ B cells are essential for maintaining self-tolerance and restraining tissue inflammation, and that Tim-1 signaling-dep

SUBMITTER: Xiao S 

PROVIDER: S-EPMC7496220 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature