{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T18:26:59Z","timestamp":1776882419462,"version":"3.51.2"},"reference-count":29,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,12,21]],"date-time":"2018-12-21T00:00:00Z","timestamp":1545350400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2019,2]]},"abstract":"Abstract<\/jats:title>Psoriasis vulgaris (PV<\/jats:styled-content>) results from activation of IL<\/jats:styled-content>\u201023\/Th17 immune pathway and is further amplified by cytokines\/chemokines from skin cells. Among skin\u2010derived pro\u2010inflammatory cytokines, IL<\/jats:styled-content>\u201036 family members are highly upregulated in PV<\/jats:styled-content> patients and play a critical role in general pustular psoriasis. However, there is limited data showing crosstalk between the IL<\/jats:styled-content>\u201023 and IL<\/jats:styled-content>\u201036 pathways in PV<\/jats:styled-content>. Herein, potential attenuation of skin inflammation in the IL<\/jats:styled-content>\u201023\u2010induced mouse model of psoriasiform dermatitis by functional inhibition of IL<\/jats:styled-content>\u201036 receptor (IL<\/jats:styled-content>\u201036R) was interrogated. Anti\u2010mouse IL<\/jats:styled-content>\u201036R monoclonal antibodies (mA<\/jats:styled-content>bs) were generated and validated in vitro by inhibiting IL<\/jats:styled-content>\u201036\u03b1\u2010induced secretion of CXCL<\/jats:styled-content>1 from NIH<\/jats:styled-content> 3T3 cells. Antibody target engagement was demonstrated by inhibition of CXCL<\/jats:styled-content>1 production in a novel acute model of IL<\/jats:styled-content>\u201036\u03b1 systemic injection in mice. In addition, anti\u2010IL<\/jats:styled-content>\u201036R mA<\/jats:styled-content>bs inhibited tissue inflammation and inflammatory gene expression in an IL<\/jats:styled-content>\u201036\u03b1 ear injection model of psoriasiform dermatitis demonstrating engagement of the target in the ear skin. To elucidate the possible role of IL<\/jats:styled-content>\u201036 signalling in IL<\/jats:styled-content>\u201023\/Th17 pathway, the ability of anti\u2010IL<\/jats:styled-content>\u201036R mA<\/jats:styled-content>bs to inhibit skin inflammation in an IL<\/jats:styled-content>\u201023 ear injection model was assessed. Inhibiting the IL<\/jats:styled-content>\u201036 pathway resulted in significant attenuation of skin thickening and psoriasis\u2010relevant gene expression. Taken together, these data suggest a role for IL<\/jats:styled-content>\u201036 signalling in the IL<\/jats:styled-content>\u201023\/Th17 signalling axis in PV.<\/jats:p>","DOI":"10.1111\/exd.13841","type":"journal-article","created":{"date-parts":[[2018,11,12]],"date-time":"2018-11-12T07:44:53Z","timestamp":1542008693000},"page":"113-120","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["IL<\/scp>\u201036 receptor antagonistic antibodies inhibit inflammatory responses in preclinical models of psoriasiform dermatitis"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4763-3361","authenticated-orcid":false,"given":"Zhi","family":"Su","sequence":"first","affiliation":[{"name":"Dermatology Discovery AbbVie Inc. 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