{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T05:36:21Z","timestamp":1793684181634,"version":"4.5.1"},"reference-count":87,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2018,9,1]],"date-time":"2018-09-01T00:00:00Z","timestamp":1535760000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Psoriasis vulgaris is a common, heterogeneous, chronic inflammatory skin disease characterized by thickened, red, scaly plaques and systemic inflammation. Psoriasis is also associated with multiple comorbid conditions, such as joint destruction, cardiovascular disease, stroke, hypertension, metabolic syndrome, and chronic kidney disease. The discovery of IL-17\u2013producing T cells in a mouse model of autoimmunity transformed our understanding of inflammation driven by T lymphocytes and associations with human inflammatory diseases, such as psoriasis. Under the regulation of IL-23, T cells that produce high levels of IL-17 create a self-amplifying, feed-forward inflammatory response in keratinocytes that drives the development of thickened skin lesions infiltrated with a mixture of inflammatory cell populations. Recently, the Food and Drug Administration approved multiple highly effective psoriasis therapies that disrupt IL-17 (secukinumab, ixekizumab, and brodalumab) and IL-23 (guselkumab and tildrakizumab) signaling in the skin, thus leading to a major paradigm shift in the way that psoriatic disease is managed.<\/jats:p>","DOI":"10.4049\/jimmunol.1800013","type":"journal-article","created":{"date-parts":[[2018,9,4]],"date-time":"2018-09-04T20:35:21Z","timestamp":1536093321000},"page":"1605-1613","source":"Crossref","is-referenced-by-count":565,"title":["Discovery of the IL-23\/IL-17 Signaling Pathway and the Treatment of Psoriasis"],"prefix":"10.1093","volume":"201","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5870-181X","authenticated-orcid":false,"given":"Jason E","family":"Hawkes","sequence":"first","affiliation":[{"name":"Laboratory for Investigative Dermatology, The Rockefeller University , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8302-5104","authenticated-orcid":false,"given":"Bernice Y","family":"Yan","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology, The Rockefeller University , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom C","family":"Chan","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology, The Rockefeller University , New York, NY 10065"},{"name":"Department of Dermatology, National Taiwan University Hospital and College of Medicine , Taipei 10002 ,","place":["Taiwan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G","family":"Krueger","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology, The Rockefeller University , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,9,15]]},"reference":[{"key":"2025030417572496600_r1","doi-asserted-by":"crossref","first-page":"512","DOI":"10.1016\/j.jaad.2013.11.013","article-title":"Psoriasis prevalence among adults in the United States","volume":"70","author":"Rachakonda","year":"2014","journal-title":"J. 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