| First Author | Hall JA | Year | 2022 |
| Journal | Immunity | Volume | 55 |
| Issue | 11 | Pages | 2027-2043.e9 |
| PubMed ID | 36243007 | Mgi Jnum | J:336987 |
| Mgi Id | MGI:7384145 | Doi | 10.1016/j.immuni.2022.09.013 |
| Citation | Hall JA, et al. (2022) Transcription factor RORalpha enforces stability of the Th17 cell effector program by binding to a Rorc cis-regulatory element. Immunity 55(11):2027-2043.e9 |
| abstractText | T helper 17 (Th17) cells regulate mucosal barrier defenses but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been elucidated, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORgammat is critical for Th17 cell differentiation; however, it is not clear whether the closely related RORalpha, which is co-expressed in Th17 cells, has a distinct role. Here, we demonstrated that although dispensable for Th17 cell differentiation, RORalpha was necessary for optimal Th17 responses in peripheral tissues. The absence of RORalpha in T cells led to reductions in both RORgammat expression and effector function among Th17 cells. Cooperative binding of RORalpha and RORgammat to a previously unidentified Rorc cis-regulatory element was essential for Th17 lineage maintenance in vivo. These data point to a non-redundant role of RORalpha in Th17 lineage maintenance via reinforcement of the RORgammat transcriptional program. |
