{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T12:57:16Z","timestamp":1762865836839,"version":"3.40.3"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T00:00:00Z","timestamp":1314835200000},"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":[[2011,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Recent studies have shown that IL-17 can contribute beneficially to pathogen defense but also that excessive IL-17 levels are associated with chronic inflammation and autoimmune disorders. To date, the role of IL-17 in viral infections and type 1 diabetes is ambiguous. In this study, we used IL-17A enhanced green fluorescent protein bicistronic reporter mouse strains to analyze in situ production of IL-17A. Upon Klebsiella pneumoniae bacterial infection, CD4+ and \u03b3\u03b4 T cells produce IL-17A. In contrast, CD4+ or CD8+ T cells do not produce IL-17A in response to acute or protracted viral infection with lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lymphocytic choriomeningitis virus-induced model of type 1 diabetes. We conclude that viral elimination and type 1 diabetes can occur in the absence of detectable IL-17A production, suggesting IL-17A is not essential in these settings.<\/jats:p>","DOI":"10.4049\/jimmunol.1000180","type":"journal-article","created":{"date-parts":[[2011,8,11]],"date-time":"2011-08-11T04:35:15Z","timestamp":1313037315000},"page":"2915-2922","source":"Crossref","is-referenced-by-count":10,"title":["Development of Autoimmune Diabetes in the Absence of Detectable IL-17A in a CD8-Driven Virally Induced Model"],"prefix":"10.1093","volume":"187","author":[{"given":"Tom L","family":"Van Belle","sequence":"first","affiliation":[{"name":"Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology , La Jolla, CA 92037"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Enric","family":"Esplugues","sequence":"additional","affiliation":[{"name":"Department of Immunobiology, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeanette","family":"Liao","sequence":"additional","affiliation":[{"name":"Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology , La Jolla, CA 92037"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Therese","family":"Juntti","sequence":"additional","affiliation":[{"name":"Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology , La Jolla, CA 92037"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard A","family":"Flavell","sequence":"additional","affiliation":[{"name":"Department of Immunobiology, Yale University School of Medicine , New Haven, CT 06520"},{"name":"Howard Hughes Medical Institute, Yale University , New Haven, CT 06520"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias G","family":"von Herrath","sequence":"additional","affiliation":[{"name":"Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology , La Jolla, CA 92037"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2011,9,15]]},"reference":[{"key":"2025032410363995600_r1","doi-asserted-by":"crossref","first-page":"821","DOI":"10.1146\/annurev.immunol.25.022106.141557","article-title":"IL-17 family cytokines and the expanding diversity of effector T cell lineages","volume":"25","author":"Weaver","year":"2007","journal-title":"Annu. 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