| First Author | Yamazaki S | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 17402 |
| PubMed ID | 29234109 | Mgi Jnum | J:287427 |
| Mgi Id | MGI:6415787 | Doi | 10.1038/s41598-017-17597-3 |
| Citation | Yamazaki S, et al. (2017) The AP-1 transcription factor JunB is required for Th17 cell differentiation. Sci Rep 7(1):17402 |
| abstractText | Interleukin (IL)-17-producing T helper (Th17) cells are crucial for host defense against extracellular microbes and pathogenesis of autoimmune diseases. Here we show that the AP-1 transcription factor JunB is required for Th17 cell development. Junb-deficient CD4(+) T cells are able to develop in vitro into various helper T subsets except Th17. The RNA-seq transcriptome analysis reveals that JunB is crucial for the Th17-specific gene expression program. Junb-deficient mice are completely resistant to experimental autoimmune encephalomyelitis, a Th17-mediated inflammatory disease, and naive T helper cells from such mice fail to differentiate into Th17 cells. JunB appears to activate Th17 signature genes by forming a heterodimer with BATF, another AP-1 factor essential for Th17 differentiation. The mechanism whereby JunB controls Th17 cell development likely involves activation of the genes for the Th17 lineage-specifying orphan receptors RORgammat and RORalpha and reduced expression of Foxp3, a transcription factor known to antagonize RORgammat function. |
