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


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 ROR?t-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 ROR?t 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-?1-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.

SUBMITTER: Hasan Z 

PROVIDER: S-EPMC5460000 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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

Hasan Zafrul Z   Koizumi Shin-Ichi SI   Sasaki Daiki D   Yamada Hayato H   Arakaki Nana N   Fujihara Yoshitaka Y   Okitsu Shiho S   Shirahata Hiroki H   Ishikawa Hiroki H  

Nature communications 20170530


CD4<sup>+</sup> T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (T<sub>H</sub>17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic T<sub>H</sub>17 subsets share a common RORγt-dependent T<sub>H</sub>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<sub>H</sub>17 pathoge  ...[more]

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