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Although a principal effector of T helper type 17 cells, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A is produced by many other cell types including <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells and \u03b3\u03b4 T cells, and is found at high levels associated with mast cells and neutrophils at sites of skin and joint disease in humans. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A up\u2010regulates expression of numerous inflammation\u2010related genes in target cells such as keratinocytes and fibroblasts, leading to increased production of chemokines, cytokines, antimicrobial peptides and other mediators that contribute to clinical disease features. Importantly, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A must be considered within the context of the local microenvironment, because it acts synergistically or additively with other pro\u2010inflammatory cytokines, including tumour necrosis factor. Several direct <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A inhibitors have shown promising activity in proof of concept and phase 2 clinical studies, thereby providing confirmation of experimental data supporting <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A in disease pathogenesis, although levels of response are not predicted by pre\u2010clinical findings. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A inhibitors produced rapid down\u2010regulation of the psoriasis gene signature and high clinical response rates in patients with moderate\u2010to\u2010severe plaque psoriasis, consistent with an important role for <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A in psoriasis pathogenesis. Clinical response rates with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A inhibitors in psoriatic arthritis and rheumatoid arthritis, however, were improved to a lesser degree compared with placebo, suggesting that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A is either important in a subset of patients or plays a relatively minor role in inflammatory joint disease. Ongoing phase 3 clinical trials should provide further information on the role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A in these diseases.<\/jats:p>","DOI":"10.1111\/imm.12142","type":"journal-article","created":{"date-parts":[[2013,7,2]],"date-time":"2013-07-02T16:03:01Z","timestamp":1372780981000},"page":"133-142","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":215,"title":["Interleukin\u201017A: a unique pathway in immune\u2010mediated diseases: psoriasis, psoriatic arthritis and rheumatoid arthritis"],"prefix":"10.1111","volume":"141","author":[{"given":"Bruce W.","family":"Kirkham","sequence":"first","affiliation":[{"name":"Department of Rheumatology Guy's &amp; St Thomas' NHS Foundation Trust London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur","family":"Kavanaugh","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Allergy and 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