| First Author | Croxford JL | Year | 2006 |
| Journal | Nat Immunol | Volume | 7 |
| Issue | 9 | Pages | 987-94 |
| PubMed ID | 16878136 | Mgi Jnum | J:112657 |
| Mgi Id | MGI:3662976 | Doi | 10.1038/ni1370 |
| Citation | Croxford JL, et al. (2006) Invariant V(alpha)19i T cells regulate autoimmune inflammation. Nat Immunol 7(9):987-94 |
| abstractText | T cells expressing an invariant V(alpha)19-J(alpha)33 T cell receptor alpha-chain (V(alpha)19i TCR) are restricted by the nonpolymorphic major histocompatibility complex class Ib molecule MR1. Whether V(alpha)19i T cells are involved in autoimmunity is not understood. Here we demonstrate that T cells expressing the V(alpha)19i TCR transgene inhibited the induction and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Similarly, EAE was exacerbated in MR1-deficient mice, which lack V(alpha)19i T cells. EAE suppression was accompanied by reduced production of inflammatory mediators and increased secretion of interleukin 10. Interleukin 10 production occurred at least in part through interactions between B cells and V(alpha)19i T cells mediated by the ICOS costimulatory molecule. These results suggest an immunoregulatory function for V(alpha)19i T cells. |
