@article{oai:oist.repo.nii.ac.jp:00000288,
 author = {Hasan, Zafrul and Koizumi, Shin-ichi and Sasaki, Daiki and Yamada, Hayato and Arakaki, Nana and Fujihara, Yoshitaka and Okitsu, Shiho and Shirahata, Hiroki and Ishikawa, Hiroki},
 journal = {Nature Communications},
 month = {May},
 note = {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 RORγt-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 RORγt 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-β1-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.},
 title = {JunB is essential for IL-23-dependent pathogenicity of Th17 cells},
 volume = {8},
 year = {2017}
}