期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 134, 期 3, 页码 728-735出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2013.404
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类别
资金
- EMBO Long Term Fellowship [ALTF 508-2011]
- FP6 Marie Curie Research Training Network [MRTN-CT-2004-005632]
- Margarethe-Waitz-Foundation Mainz
- MAIFOR
- Stiftung Mainzer Herz
- DFG [WA1600/6-1, FOR1336, SFB/TR 128, SFB490, Ste 833/6-2, 11-1]
- Immunology Center of Excellence Mainz (FZI)
The lack of a generally accepted animal model for human psoriasis has hindered progress with respect to understanding the pathogenesis of the disease. Here we present a model in which transgenic IL-17A expression is targeted to the skin in mice, achievable after crossing our IL-17A(ind) allele to the K14-Cre strain. K14-IL-17A(ind/+) mice invariably develop an overt skin inflammation bearing many hallmark characteristics of human psoriasis including dermal infiltration of effector T cells, formation of neutrophil nnicroabscesses, and hyperkeratosis. IL-17A expression in the skin results in upregulated granulopoiesis and migration of IL-6R-expressing neutrophils into the skin. Neutralization of IL-6 signaling efficiently reduces the observed pathogenesis in skin of IL-17A-overexpressing mice, with marked reductions in epidermal neutrophil abscess formation and epidermal thickening. Thus, IL-6 functions downstream of IL-17A to exacerbate neutrophil microabscess development in psoriasiform lesions.
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