{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T16:42:15Z","timestamp":1777999335702,"version":"3.51.4"},"reference-count":18,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"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":[[2016,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>IL-1\u03b2 is a proinflammatory cytokine important for local and systemic immunity. However, aberrant production of this cytokine is implicated in pathogenic mechanisms of a number of inflammatory diseases, including Beh\u00e7et\u2019s disease and age-related macular degeneration. In this study, we report the increased secretion of IL-1\u03b2 in the retina by neutrophils, macrophages, and dendritic cells during ocular inflammation and show that loss of IL-1R signaling confers protection from experimental autoimmune uveitis. Moreover, the amelioration of experimental autoimmune uveitis in Il1r-deficient mice was associated with reduced infiltration of inflammatory cells into the retina and decreased numbers of uveitogenic Th17 cells that mediate uveitis. These findings indicate the possible utility of IL-1R\u2013blocking agents for the treatment of ocular inflammatory diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.1502080","type":"journal-article","created":{"date-parts":[[2015,12,8]],"date-time":"2015-12-08T14:29:59Z","timestamp":1449584999000},"page":"543-546","source":"Crossref","is-referenced-by-count":42,"title":["Cutting Edge: IL-1 Receptor Signaling is Critical for the Development of Autoimmune Uveitis"],"prefix":"10.1093","volume":"196","author":[{"given":"Chi-Keung","family":"Wan","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1178-5950","authenticated-orcid":false,"given":"Chang","family":"He","sequence":"additional","affiliation":[{"name":"Molecular Immunology Section, National Eye Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Sun","sequence":"additional","affiliation":[{"name":"Molecular Immunology Section, National Eye Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9986-3839","authenticated-orcid":false,"given":"Charles E","family":"Egwuagu","sequence":"additional","affiliation":[{"name":"Molecular Immunology Section, National Eye Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Warren J","family":"Leonard","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2016,1,15]]},"reference":[{"key":"2025030702114817000_r1","doi-asserted-by":"crossref","first-page":"711","DOI":"10.1038\/nm1585","article-title":"TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27\/STAT1","volume":"13","author":"Amadi-Obi","year":"2007","journal-title":"Nat. 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