| First Author | Noubade R | Year | 2007 |
| Journal | J Clin Invest | Volume | 117 |
| Issue | 11 | Pages | 3507-18 |
| PubMed ID | 17965772 | Mgi Jnum | J:127383 |
| Mgi Id | MGI:3763670 | Doi | 10.1172/JCI32792 |
| Citation | Noubade R, et al. (2007) Histamine receptor H1 is required for TCR-mediated p38 MAPK activation and optimal IFN-gamma production in mice. J Clin Invest 117(11):3507-18 |
| abstractText | Histamine receptor H1 (H1R) is a susceptibility gene in both experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune orchitis (EAO), 2 classical T cell-mediated models of organ-specific autoimmune disease. Here we showed that expression of H1R in naive CD4+ T cells was required for maximal IFN-gamma production but was dispensable for proliferation. Moreover, H1R signaling at the time of TCR ligation was required for activation of p38 MAPK, a known regulator of IFN-gamma expression. Importantly, selective reexpression of H1R in CD4+ T cells fully complemented both the IFN-gamma production and the EAE susceptibility of H1R-deficient mice. These data suggest that the presence of H1R in CD4+ T cells and its interaction with histamine regulates early TCR signals that lead to Th1 differentiation and autoimmune disease. |
