| First Author | Nakajima S | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 8 | Pages | 2122-2130 |
| PubMed ID | 24480880 | Mgi Jnum | J:212778 |
| Mgi Id | MGI:5582144 | Doi | 10.1038/jid.2014.51 |
| Citation | Nakajima S, et al. (2014) IL-17A as an inducer for Th2 immune responses in murine atopic dermatitis models. J Invest Dermatol 134(8):2122-30 |
| abstractText | Atopic dermatitis (AD) is generally regarded as a type 2 helper T (Th2)-mediated inflammatory skin disease. Although the number of IL-17A-producing cells is increased in the peripheral blood and in acute skin lesion of AD patients, the role of IL-17A in the pathogenesis of AD remains unclear. To clarify this issue, we used murine AD models in an IL-17A-deficient condition. In a repeated hapten application-induced AD model, skin inflammation, IL-4 production in the draining lymph nodes (LNs), and hapten-specific IgG1 and IgE induction were suppressed in IL-17A-deficient mice. Vgamma4(+) gammadelta T cells in the skin-draining LNs and Vgamma5(-) dermal gammadelta T cells in the skin were the major sources of IL-17A. Consistently, in flaky-tail (Flg(ft/ft) ma/ma) mice, spontaneous development of AD-like dermatitis and IgE induction were attenuated by IL-17A deficiency. Moreover, Th2 differentiation from naive T cells was promoted in vitro by the addition of IL-17A. Taken together, our results suggest that IL-17A mediates Th2-type immune responses and that IL-17A signal may be a therapeutic target of AD. |
