| First Author | Xiao S | Year | 2020 |
| Journal | Cell Rep | Volume | 32 |
| Issue | 2 | Pages | 107892 |
| PubMed ID | 32668241 | Mgi Jnum | J:301616 |
| Mgi Id | MGI:6489166 | Doi | 10.1016/j.celrep.2020.107892 |
| Citation | Xiao S, et al. (2020) Checkpoint Receptor TIGIT Expressed on Tim-1(+) B Cells Regulates Tissue Inflammation. Cell Rep 32(2):107892 |
| abstractText | 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-dependent TIGIT expression on B cells is essential for maintaining CNS-specific tolerance. A possible critical role of aryl hydrocarbon receptor (AhR) in regulating the B cell function is discussed, as we find that AhR is among the preferentially expressed transcription factors in Tim-1(+) B cells and regulates their TIGIT and IL-10 expression. |
