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10.7150/ijms.20809

http://scihub22266oqcxt.onion/10.7150/ijms.20809
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C5599924!5599924!28924372
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suck abstract from ncbi


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pmid28924372      Int+J+Med+Sci 2017 ; 14 (10): 1002-7
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  • IL-36? inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis #MMPMID28924372
  • Wang W; Yu X; Wu C; Jin H
  • Int J Med Sci 2017[]; 14 (10): 1002-7 PMID28924372show ga
  • Psoriasis is a common inflammatory skin disease characterized by abnormal keratinocyte inflammation and differentiation that has a major impact on patients' quality of life. IL-36?, a member of IL-36 cytokine family, is highly expressed in psoriasis and plays an important role in inflammation response and differentiation. However, the function of IL-36? in differentiation and inflammation of keratinocyte in psoriasis has not been clearly identified. Thus, this study aimed to investigate the role of IL-36? on differentiation and inflammation in HaCaT cells. HaCaT cells were divided into three groups: (1) Control group; (2) IL-36? (100 ng/mL) group; (3) IL-36? (100 ng/mL) + IWP-2 (1?M) group. Real time PCR was used to detect gene expression; the inflammation cytokines were examined by ELISA. We showed that treatment of HaCaT cells with IL-36? significantly upregulated the expression levels of ?-catenin, cyclin D1, and ki-67. IL-36? also promoted the production of the inflammatory cytokines IFN-?, IL-1? and IL-6, suppressed the expression of filaggrin, involucrin, keratin 1 and keratin 5. Meanwhile, we demonstrated the role of IWP-2, an inhibitor of the Wnt signaling pathway, in IL-36?-treated HaCaT cells. Collectively, our findings suggest that IL-36? inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis, this indicated that downregulation of IL-36? may be a potential therapeutic option in psoriasis.
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