@article{8cadcc81fa4246bda595f10b6509eae2,
title = "The AP-1 transcription factor JunB is required for Th17 cell differentiation",
abstract = "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 RORγt and RORα and reduced expression of Foxp3, a transcription factor known to antagonize RORγt function.",
author = "Soh Yamazaki and Yoshihiko Tanaka and Hiromitsu Araki and Akira Kohda and Fumiyuki Sanematsu and Tomoko Arasaki and Xuefeng Duan and Fumihito Miura and Takaharu Katagiri and Ryodai Shindo and Hiroyasu Nakano and Takashi Ito and Yoshinori Fukui and Shogo Endo and Hideki Sumimoto",
note = "Funding Information: We thank Masako Suzuki, Yoko Kage, and Namiko Kubo for technical assistance, Drs Naoko Satoh and Hiroshi Ohno (RIKEN) for advise on preparation of lamina propria lymphocytes from mouse short intestine, and Dr. Riko Nishimura (Osaka University) for advise on an osteoclast differentiation experiment; and technical supports from Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences, from the Laboratory for Technical Support, Medical Institute of Bioregulation, Kyushu University, and from Advanced Medical Research Center, Toho University Graduate School of Medicine. MS12 cells were a generous gift from the Meiji Dairies Corporation. This work was supported in part by grants from MEXT (the Ministry of Education, Culture, Sports, Science and Technology), from JSPS (Japan Society for the Promotion of Science: a Grant-in-Aid for Scientific Research on Innovative Areas “Oxygen Biology: a new criterion for integrated understanding of life” No. 26111009), from a Grant-in Aid for Scientific Research (C) (23590338 to S.Y.), from the Research Promotion Grant from Toho University Graduate School of Medicine (No.17-02 to S.Y.), from Private University Research Branding project (to H.N.) from the MEXT, and from the Naito Foundation; and by the Platform Project for Supporting in Drug Discovery and Life Science Research (Platform for Drug Discovery, Informatics, and Structural Life Science) from AMED (Japan Agency for Medical Research and Development). Publisher Copyright: {\textcopyright} 2017 The Author(s).",
year = "2017",
month = dec,
day = "1",
doi = "10.1038/s41598-017-17597-3",
language = "English",
volume = "7",
journal = "Scientific reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",
}