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- W4313356022 abstract "Abstract IL-22 plays an important role in modulation of tissue repair and inflammatory responses and is implicated in psoriasis, ulcerative colitis, as well as liver and pancreas damage. The molecular mechanisms of its regulation have been actively studied. In our study, STAT1 but not T-bet deficiency resulted in higher levels of IL-22 expression and severer acanthosis in imiquimod-induced mouse psoriasiform skin inflammation, which indicates a critical role of STAT1 in repressing IL-22 gene expression and psoriasis pathogenesis. Quantitative RT-PCR data showed that high levels of IL-22 production were only observed in STAT1 but not T-bet deficient T cells stimulated with anti-CD3 and anti-CD28 in combination with or without IL-6 plus IL-23, further demonstrating that STAT1 but not T-bet is crucial to suppress IL-22 gene expression. There was no difference between STAT1 and T-bet deficiency in activation of transcription factors RORγt, c-Maf, ICOS or AhR, suggesting they do not play significant roles in STAT1 mediated IL-22 inhibition. A STAT binding motif was identified within IL-22 promoter, and CHIP assay showed direct interaction between STAT1 and IL-22 promoters, revealing a novel regulatory mechanism of IL-22 suppression by STAT1. Additional molecular mechanisms of STAT1 mediated IL-22 regulation are currently under investigation." @default.
- W4313356022 created "2023-01-06" @default.
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- W4313356022 date "2017-05-01" @default.
- W4313356022 modified "2023-09-30" @default.
- W4313356022 title "STAT1 activation represses IL-22 gene expression and psoriasis pathogenesis." @default.
- W4313356022 doi "https://doi.org/10.4049/jimmunol.198.supp.124.18" @default.
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