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Sci Rep. 2017 Dec 12;7(1):17402. doi: 10.1038/s41598-017-17597-3.

The AP-1 transcription factor JunB is required for Th17 cell differentiation.

Author information

1
Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka, 812-8582, Japan.
2
Department of Biochemistry, Toho University School of Medicine, Tokyo, 143-8540, Japan.
3
Division of Immunogenetics, Department of Immunobiology of Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
4
Section of Infection Biology, Department of Functional Bioscience, Fukuoka Dental College, Fukuoka, 814-0193, Japan.
5
Aging Neuroscience Research Team, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
6
Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka, 812-8582, Japan. hsumi@med.kyushu-u.ac.jp.

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.

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