| First Author | Hasan Z | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 15628 | PubMed ID | 28555647 |
| Mgi Jnum | J:244764 | Mgi Id | MGI:5913543 |
| Doi | 10.1038/ncomms15628 | Citation | Hasan Z, et al. (2017) JunB is essential for IL-23-dependent pathogenicity of Th17 cells. Nat Commun 8:15628 |
| abstractText | CD4+ T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (TH17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic TH17 subsets share a common RORgammat-dependent TH17 transcriptional programme, transcriptional regulatory mechanisms specific to each of these subsets are mostly unknown. Here we show that the AP-1 transcription factor JunB is critical for TH17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of RORgammat and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic TH17 cells, but not in TGF-beta1-dependent non-pathogenic TH17 cells. Junb-deficient T cells fail to induce TH17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic TH17 cells. The selective requirement of JunB for IL-23-dependent TH17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases. |
