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JunB is essential for IL-23-dependent pathogenicity of Th17 cells

Author

Listed:
  • Zafrul Hasan

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Shin-ichi Koizumi

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Daiki Sasaki

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Hayato Yamada

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Nana Arakaki

    (DNA Sequencing Section, Okinawa Institute of Science and Technology Graduate University)

  • Yoshitaka Fujihara

    (Research Institute for Microbial Diseases, Osaka University)

  • Shiho Okitsu

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Hiroki Shirahata

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

  • Hiroki Ishikawa

    (Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University)

Abstract

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.

Suggested Citation

  • Zafrul Hasan & Shin-ichi Koizumi & Daiki Sasaki & Hayato Yamada & Nana Arakaki & Yoshitaka Fujihara & Shiho Okitsu & Hiroki Shirahata & Hiroki Ishikawa, 2017. "JunB is essential for IL-23-dependent pathogenicity of Th17 cells," Nature Communications, Nature, vol. 8(1), pages 1-12, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15628
    DOI: 10.1038/ncomms15628
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    Cited by:

    1. Jiacheng Hao & Chang Liu & Zhijie Gu & Xuanming Yang & Xun Lan & Xiaohuan Guo, 2024. "Dysregulation of Wnt/β-catenin signaling contributes to intestinal inflammation through regulation of group 3 innate lymphoid cells," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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