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

Autor: 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
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Zdroj: Scientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
Druh dokumentu: article
ISSN: 2045-2322
DOI: 10.1038/s41598-018-25094-4
Popis: Abstract 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.
Databáze: Directory of Open Access Journals
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje