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10.1038/s41598-018-25094-4

http://scihub22266oqcxt.onion/10.1038/s41598-018-25094-4
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C5923199!5923199!29703903
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suck abstract from ncbi


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pmid29703903      Sci+Rep 2018 ; 8 (ä): ä
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  • IL-31 is crucial for induction of pruritus, but not inflammation, in contact hypersensitivity #MMPMID29703903
  • Takamori A; Nambu A; Sato K; Yamaguchi S; Matsuda K; Numata T; Sugawara T; Yoshizaki T; Arae K; Morita H; Matsumoto K; Sudo K; Okumura K; Kitaura J; Matsuda H; Nakae S
  • Sci Rep 2018[]; 8 (ä): ä PMID29703903show ga
  • IL-31, which is a member of the IL-6 family of cytokines, is produced mainly by activated CD4+ T cells, in particular activated Th2 cells, suggesting a contribution to development of type-2 immune responses. IL-31 was reported to be increased in specimens from patients with atopic dermatitis, and IL-31-transgenic mice develop atopic dermatitis-like skin inflammation, which is involved in the pathogenesis of atopic dermatitis. However, the role of IL-31 in development of contact dermatitis/contact hypersensitivity (CHS), which is mediated by hapten-specific T cells, including Th2 cells, is not fully understood. Therefore, we investigated this using IL-31-deficient (Il31?/?) mice, which we newly generated. We demonstrated that the mice showed normal migration and maturation of skin dendritic cells and induction of hapten-specific T cells in the sensitization phase of FITC-induced CHS, and normal induction of local inflammation in the elicitation phase of FITC- and DNFB-induced CHS. On the other hand, those mice showed reduced scratching frequency and duration during FITC- and/or DNFB-induced CHS. Our findings suggest that IL-31 is responsible for pruritus, but not induction of local skin inflammation, during CHS induced by FITC and DNFB.
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