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

Soh Yamazaki, Yoshihiko Tanaka, Hiromitsu Araki, Akira Kohda, Fumiyuki Sanematsu, Tomoko Arasaki, Xuefeng Duan, Fumihito Miura, Takaharu Katagiri, Ryodai Shindo, Hiroyasu Nakano, Takashi Ito, Yoshinori Fukui, Shogo Endo, Hideki Sumimoto

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)

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.

Original languageEnglish
Article number17402
JournalScientific reports
Volume7
Issue number1
DOIs
Publication statusPublished - Dec 1 2017

All Science Journal Classification (ASJC) codes

  • General

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