| First Author | Ying H | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 3 | Pages | 1375-8 |
| PubMed ID | 20601598 | Mgi Jnum | J:162452 |
| Mgi Id | MGI:4819015 | Doi | 10.4049/jimmunol.0903369 |
| Citation | Ying H, et al. (2010) Cutting edge: CTLA-4-B7 interaction suppresses Th17 cell differentiation. J Immunol 185(3):1375-8 |
| abstractText | Th cells that produce IL-17 (Th17 cells) are a distinct subset of Th cells implicated in several autoimmune diseases. Although CD28-B7 interaction has been shown to be involved in Th17 differentiation in vitro, the role of CTLA-4 in controlling Th17 development is completely unknown. We report in this paper that blocking the CTLA-4-B7 interaction potentiates Th17 cell differentiation in vitro and in vivo. Furthermore, blocking CTLA-4-B7 interaction in vivo confers the susceptibility of experimental autoimmune myocarditis to CD28(-/-) mice or increases the severity of experimental autoimmune myocarditis in wild-type mice. The enhanced disease susceptibility is mediated by heightened Th17 responses. With these results, we are the first to demonstrate that CTLA-4-B7 interaction inhibits Th17 differentiation in vitro and in vivo and suppresses Th17-mediated autoimmunity. |
