論文

査読有り 国際誌
2018年4月27日

IL-31 is crucial for induction of pruritus, but not inflammation, in contact hypersensitivity.

Scientific reports
  • Ayako Takamori
  • ,
  • Aya Nambu
  • ,
  • Keiko Sato
  • ,
  • Sachiko Yamaguchi
  • ,
  • Kenshiro Matsuda
  • ,
  • Takafumi Numata
  • ,
  • Takeru Sugawara
  • ,
  • Takamichi Yoshizaki
  • ,
  • Ken Arae
  • ,
  • Hideaki Morita
  • ,
  • Kenji Matsumoto
  • ,
  • Katsuko Sudo
  • ,
  • Ko Okumura
  • ,
  • Jiro Kitaura
  • ,
  • Hiroshi Matsuda
  • ,
  • Susumu Nakae

8
1
開始ページ
6639
終了ページ
6639
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-018-25094-4

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.

リンク情報
DOI
https://doi.org/10.1038/s41598-018-25094-4
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/29703903
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5923199

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