期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 133, 期 2, 页码 441-451出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2012.318
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资金
- Margarethe-Waitz-Foundation Mainz
- Hertie Foundation
- DFG [SFB/TR 52, AW1600/6-1]
- Research Center of Immunology Mainz (FZI)
Topical application of imiquimod (IMQ) on the skin of mice induces inflammation with common features found in psoriatic skin. Recently, it was postulated that IL-17 has an important role both in psoriasis and in the IMQ model. To further investigate the impact of IL-17RA signaling in psoriasis, we generated IL-17 receptor A (IL-17RA)-deficient mice (IL-17RA(del)) and challenged these mice with IMQ. Interestingly, the disease was only partially reduced and delayed but not abolished when compared with controls. In the absence of IL-17RA, we found persisting signs of inflammation such as neutrophil and macrophage infiltration within the skin. Surprisingly, already in the naive state, the skin of IL-17RA(del) mice contained significantly elevated numbers of Th17- and IL-17-producing gamma delta T cells, assuming that IL-17RA signaling regulates the population size of Th17 and gamma delta T cells. Upon IMQ treatment of IL-17RA(del) mice, these cells secreted elevated amounts of tumor necrosis factor-alpha, IL-6, and IL-22, accompanied by increased levels of the chemokine CXCL2, suggesting an alternative pathway of neutrophil and macrophage skin infiltration. Hence, our findings have major implications in the potential long-term treatment of psoriasis by IL-17-targeting drugs. Journal of Investigative Dermatology (2013) 133, 441-451; doi:10.1038/jid.2012.318; published online 6 September 2012
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