期刊
JOURNAL OF DERMATOLOGICAL SCIENCE
卷 96, 期 1, 页码 2-7出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jdermsci.2019.08.006
关键词
Group 2 innate lymphoid cells (ILC2s); Basophils; IL-4; IL-33; Atopic dermatitis
类别
资金
- JSPS KAKENHI [18K08284]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [18K08284] Funding Source: KAKEN
Atopic dermatitis (AD) is characterized by pruritus, barrier disruption, and inflammation including type 2 cytokine production. Interleukin-33 (IL-33) is an inflammatory cytokine that is over-expressed in the keratinocytes of patients with AD. IL-33 transgenic mice, which express IL-33 specifically in keratinocytes, spontaneously develop AD-like eczema, suggesting that IL-33 is sufficient for the development of AD. IL-33 stimulates various cells, including group 2 innate lymphoid cells (ILC2s), to produce type 2 cytokines, such as IL-5 and IL-13, and IL-33-stimulated basophils activate ILC2s via IL-4. ILC2s are enriched in human AD skin lesions, and ILC2 isolated from AD lesions, are activated by IL-33, not by thymic stromal lymphopoietin (TSLP). IL-33 induces IL-31, thereby promoting pruritus and scratching behavior. Conversely, scratching the skin promotes IL-33 release from keratinocytes. IL-33 reduces the expression of filaggrin and claudin-1; it also reduces the skin barrier function. However, barrier destruction causes percutaneous exposure to allergens or IL-33 release. Thus, IL-33 is a common point of entry into the itch-scratch cycle of AD. These new findings can facilitate the development of novel therapeutic drugs targeting IL-33. (C) 2019 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.
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