期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 134, 期 8, 页码 2122-2130出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2014.51
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资金
- Ministries of Education, Culture, Sports, Science and Technology
- Janssen Pharmaceutical
- Japan Society for the Promotion of Science
- Grants-in-Aid for Scientific Research [13J02446] Funding Source: KAKEN
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. V gamma 4(+) gamma delta T cells in the skin-draining LNs and V gamma 5(-) dermal gamma delta T cells in the skin were the major sources of IL-17A. Consistently, in flaky-tail (Fig(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.
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