{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T12:06:25Z","timestamp":1779105985995,"version":"3.51.4"},"reference-count":36,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,2,12]],"date-time":"2019-02-12T00:00:00Z","timestamp":1549929600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Zhejiang Science and Technology Bureau grant","award":["2016C33235"],"award-info":[{"award-number":["2016C33235"]}]},{"name":"Nature Science Fund of Shanghai","award":["17ZR1425700"],"award-info":[{"award-number":["17ZR1425700"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Skin injury can trigger formation of new lesions in psoriasis (Koebner phenomenon). The mechanisms through which injury exacerbates psoriasis are unclear. During wound repair, epidermal keratinocytes are activated and produce abundant <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3, further promoting the skin inflammation. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A is the cornerstone cytokine in the pathogenesis of psoriasis. We sought to investigate the effects of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A on injury\u2010induced keratinocyte activation and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 production. Here, we demonstrated that ds<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> released from necrotic keratinocytes induced the expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3. Silencing of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>3 by si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> decreased the <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 induction by necrotic keratinocyte supernatant. Co\u2010stimulation with ds<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A synergistically increased the expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 and other proinflammatory mediators (<jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>20, <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>8, <jats:styled-content style=\"fixed-case\">DEFB<\/jats:styled-content>4 and <jats:styled-content style=\"fixed-case\">LCN<\/jats:styled-content>2) in keratinocytes. The synergistic effects were not dependent on <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>3 upregulation, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content> receptor signalling and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> stabilization. Co\u2010stimulation with ds<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A resulted in an accumulation of I\u03baB\u03b6. The synergistic upregulation of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 and proinflammatory mediators were inhibited by I\u03baB\u03b6 si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>. Co\u2010stimulation with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A and poly(I:C) markedly activated the p38 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB pathway, compared with poly(I:C). Blockade of p38 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB suppressed ds<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A\u2013mediated I\u03baB\u03b6 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 induction. These findings demonstrated that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A synergistically enhanced the ds<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010mediated <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 production through a p38 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>\u2010, <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB\u2013, and I\u03baB\u03b6\u2010dependent mechanism.<\/jats:p>","DOI":"10.1111\/exd.13871","type":"journal-article","created":{"date-parts":[[2019,1,8]],"date-time":"2019-01-08T20:27:13Z","timestamp":1546979233000},"page":"233-239","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["<scp>IL<\/scp>\u201017A synergistically enhances <scp>TLR<\/scp>3\u2010mediated <scp>IL<\/scp>\u201036\u03b3 production by keratinocytes: A potential role in injury\u2010amplified psoriatic inflammation"],"prefix":"10.1111","volume":"28","author":[{"given":"Shuangchun","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Blood Transfusion Taizhou Municipal Hospital  Taizhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fei","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Shanghai Skin Disease Hospital  Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zongzhou","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Shanghai Skin Disease Hospital  Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Dermatology Shanghai Skin Disease Hospital  Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shujie","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Visual Impairment and Restoration Eye Institute Eye and ENT Hospital of Fudan University  Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7140-5505","authenticated-orcid":false,"given":"Ning","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Shanghai Skin Disease Hospital  Shanghai 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