| First Author | Melton AC | Year | 2010 |
| Journal | J Clin Invest | Volume | 120 |
| Issue | 12 | Pages | 4436-44 |
| PubMed ID | 21099117 | Mgi Jnum | J:171861 |
| Mgi Id | MGI:5000200 | Doi | 10.1172/JCI43786 |
| Citation | Melton AC, et al. (2010) Expression of alphavbeta8 integrin on dendritic cells regulates Th17 cell development and experimental autoimmune encephalomyelitis in mice. J Clin Invest 120(12):4436-44 |
| abstractText | Th17 cells promote a variety of autoimmune diseases, including psoriasis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. TGF-beta is required for conversion of naive T cells to Th17 cells, but the mechanisms regulating this process are unknown. Integrin alphavbeta8 on DCs can activate TGF-beta, and this process contributes to the development of induced Tregs. Here, we have now shown that integrin alphavbeta8 expression on DCs plays a critical role in the differentiation of Th17 cells. Th17 cells were nearly absent in the colons of mice lacking alphavbeta8 expression on DCs. In addition, these mice and the DCs harvested from them had an impaired ability to convert naive T cells into Th17 cells in vivo and in vitro, respectively. Importantly, mice lacking alphavbeta8 on DCs showed near-complete protection from experimental autoimmune encephalomyelitis. Our results therefore suggest that the integrin alphavbeta8 pathway is biologically important and that alphavbeta8 expression on DCs could be a therapeutic target for the treatment of Th17-driven autoimmune disease. |
