期刊
JOURNAL OF IMMUNOLOGY
卷 197, 期 11, 页码 4403-4412出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1600383
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资金
- National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health [AR62173]
- Shriners Hospitals for Children Grant [250862]
- National Psoriasis Foundation Translational Research Grant
IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders. However, because IL-17A is mainly produced by alpha beta and gamma delta T cells in response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A-independent actions. In this article, we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r(-/-)Rag1(-/-)- and Tcr delta-deficient mice, which can be prevented by neutrophil depletion. Moreover, adoptive transfer of CD11b(+)Gr-1(hi) cells, after IL-17A gene transfer, was sufficient to phenocopy the disease. We further show that the IL-17A-induced pathology was prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with conditional deletion of the master regulator of selective autophagy, Wdfy3. Our data demonstrate a novel T cell-independent mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia.
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