| First Author | Hilliard BA | Year | 2002 |
| Journal | J Clin Invest | Volume | 110 |
| Issue | 6 | Pages | 843-50 |
| PubMed ID | 12235116 | Mgi Jnum | J:79107 |
| Mgi Id | MGI:2387232 | Doi | 10.1172/JCI15254 |
| Citation | Hilliard BA, et al. (2002) Critical roles of c-Rel in autoimmune inflammation and helper T cell differentiation. J Clin Invest 110(6):843-50 |
| abstractText | Different members of the Rel/NF-kappaB family may play different roles in immunity and inflammation. We report here that c-Rel-deficient mice are resistant to autoimmune encephalomyelitis and are defective in Th1, but not Th2 responses. The Th1 deficiency appears to be caused by selective blockade of IL-12 production by c-Rel-deficient antigen-presenting cells, as well as by a complete abrogation of IFN-gamma expression in c-Rel-deficient T cells. Interestingly, c-Rel deficiency does not affect T-bet expression, suggesting that c-Rel may act downstream of T-bet during Th1 cell differentiation. Thus, unlike NF-kappaB1, which selectively regulates Th2 cell differentiation, c-Rel is essential for Th1 cell differentiation and Th1 cell-mediated autoimmune inflammation. |
