| First Author | Takamori A | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 6639 |
| PubMed ID | 29703903 | Mgi Jnum | J:263831 |
| Mgi Id | MGI:6162705 | Doi | 10.1038/s41598-018-25094-4 |
| Citation | Takamori A, et al. (2018) IL-31 is crucial for induction of pruritus, but not inflammation, in contact hypersensitivity. Sci Rep 8(1):6639 |
| abstractText | 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. |
