| First Author | Tang L | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 770402 | PubMed ID | 35095844 |
| Mgi Jnum | J:319730 | Mgi Id | MGI:6864846 |
| Doi | 10.3389/fimmu.2021.770402 | Citation | Tang L, et al. (2021) Tim-3 Relieves Experimental Autoimmune Encephalomyelitis by Suppressing MHC-II. Front Immunol 12:770402 |
| abstractText | Tim-3, an immune checkpoint inhibitor, is widely expressed on the immune cells and contributes to immune tolerance. However, the mechanisms by which Tim-3 induces immune tolerance remain to be determined. Major histocompatibility complex II (MHC-II) plays a key role in antigen presentation and CD4(+)T cell activation. Dysregulated expressions of Tim-3 and MHC-II are associated with the pathogenesis of many autoimmune diseases including multiple sclerosis. Here we demonstrated that, by suppressing MHC-II expression in macrophages via the STAT1/CIITA pathway, Tim-3 inhibits MHC-II-mediated autoantigen presentation and CD4(+)T cell activation. As a result, overexpression or blockade of Tim-3 signaling in mice with experimental autoimmune encephalomyelitis (EAE) inhibited or increased MHC-II expression respectively and finally altered clinical outcomes. We thus identified a new mechanism by which Tim-3 induces immune tolerance in vivo and regulating the Tim-3-MHC-II signaling pathway is expected to provide a new solution for multiple sclerosis treatment. |
