| First Author | Ruan Q | Year | 2011 |
| Journal | J Exp Med | Volume | 208 |
| Issue | 11 | Pages | 2321-33 |
| PubMed ID | 22006976 | Mgi Jnum | J:178764 |
| Mgi Id | MGI:5300106 | Doi | 10.1084/jem.20110462 |
| Citation | Ruan Q, et al. (2011) The Th17 immune response is controlled by the Rel-RORgamma-RORgamma T transcriptional axis. J Exp Med 208(11):2321-33 |
| abstractText | The Th17 cells use the retinoid-related orphan receptor-gamma (Rorg or Rorc) to specify their differentiation and lineage-specific function. However, how Rorg is switched on during Th17 differentiation is unknown. We report here that c-Rel and RelA/p65 transcription factors drive Th17 differentiation by binding to and activating two distinct Rorg promoters that control RORgammaT and RORgamma expression, respectively. Similar to RORgammaT, RORgamma is selectively expressed in Th17 cells and is effective in specifying the Th17 phenotype. T cells deficient in c-Rel or RelA are significantly compromised in Th17 differentiation, and c-Rel-deficient mice are defective in Th17 responses. Thus, Th17 immunity is controlled by a Rel-RORgamma-RORgammaT axis, and strategies targeting Rel/NF-kappaB can be effective for controlling Th17 cell-mediated diseases. |
