2017年5月
JunB is essential for IL-23-dependent pathogenicity of Th17 cells
NATURE COMMUNICATIONS
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- 巻
- 8
- 号
- 開始ページ
- 15628
- 終了ページ
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1038/ncomms15628
- 出版者・発行元
- NATURE PUBLISHING GROUP
CD4(+) T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (T(H)17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic T(H)17 subsets share a common ROR gamma t-dependent T(H)17 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 T(H)17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of ROR gamma t and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic T(H)17 cells, but not in TGF-beta 1-dependent non-pathogenic T(H)17 cells. Junb-deficient T cells fail to induce T(H)17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic T(H)17 cells. The selective requirement of JunB for IL-23-dependent T(H)17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases.
- リンク情報
- ID情報
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- DOI : 10.1038/ncomms15628
- ISSN : 2041-1723
- PubMed ID : 28555647
- Web of Science ID : WOS:000402304200001