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However why IL-17 cytokines should be so central is not known, because target cells and their functions have not been clearly delineated. Here we demonstrate that IL-17 signaling into nonkeratinocytes, specifically dermal fibroblasts, induces mediators that further increase IL-17 production by innate \u03b3\u03b4T cells and promote cellular infiltration, whereas IL-17 signaling into keratinocytes aids proliferation and blocks their differentiation. These findings reveal the circuitry underpinning critical disease-driving effects of IL-17.<\/jats:p>","DOI":"10.1073\/pnas.1400513111","type":"journal-article","created":{"date-parts":[[2014,8,5]],"date-time":"2014-08-05T02:19:13Z","timestamp":1407205153000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":163,"title":["IL-17 drives psoriatic inflammation via distinct, target cell-specific mechanisms"],"prefix":"10.1073","volume":"111","author":[{"given":"Hye-Lin","family":"Ha","sequence":"first","affiliation":[{"name":"Immune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongshan","family":"Wang","sequence":"additional","affiliation":[{"name":"Immune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious 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