期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 143, 期 1, 页码 13-25出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2018.11.014
关键词
Atopic dermatitis; genetically defined mouse models; skin barrier; immune dysfunction; T(H)2 cell response; pruritis; microbiome
资金
- JSPS KAKENHI [18F18096]
- Funding for Research to Expedite Effective drug discovery by Goverment, Academia and Private partnership (GAPFREE2) [100160600081]
- Advanced Research & Development Programs for Medical Innovation (AMED-PRIME) [18m6010014h0002]
- Grants-in-Aid for Scientific Research [18F18096] Funding Source: KAKEN
Atopic dermatitis (AD) is characterized by severe pruritus and recurrent eczema with a chronic disease course. Impaired skin barrier function, hyperactivated T(H)2 cell-type inflammation, and pruritus-induced scratching contribute to the disease pathogenesis of AD. Skin microbial alterations complicate the pathogenesis of AD further. Mouse models are a powerful tool to analyze such intricate pathophysiology of AD, with a caution that anatomy and immunology of the skin differ between human subjects and mice. Here we review recent understanding of AD etiology obtained using mouse models, which address the epidermal barrier, skin microbiome, T-H(2) immune response, and pruritus.
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