{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T18:22:21Z","timestamp":1792002141109,"version":"4.4.0"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2002,10,1]],"date-time":"2002-10-01T00:00:00Z","timestamp":1033430400000},"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":[[2002,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Spontaneous autoimmune thyroiditis (SAT) is an organ-specific autoimmune disease characterized by chronic inflammation of the thyroid by T and B lymphocytes. To investigate the roles of Th1 and Th2 cytokines in the pathogenesis of SAT, IFN-\u03b3\u2212\/\u2212 and IL-4\u2212\/\u2212 NOD.H-2h4 mice were generated. IL-4\u2212\/\u2212 mice developed lymphocytic SAT (L-SAT) comparable to that of wild-type (WT) mice. They produced little anti-mouse thyroglobulin (MTg) IgG1, but had levels of anti-MTg IgG2b comparable to WT mice. Compared with WT mice, IFN-\u03b3\u2212\/\u2212 mice produced significantly less anti-MTg IgG1 and IgG2b. Absence of IFN-\u03b3 resulted in abnormal proliferation of thyroid epithelial cells with minimal lymphocyte infiltration. Thyroids of IFN-\u03b3\u2212\/\u2212 mice had markedly reduced B lymphocyte chemoattractant expression, B cell and plasma cell infiltration, and decreased MHC class II expression on thyrocytes compared with WT mice. Adoptive transfer of WT splenocytes to IFN-\u03b3\u2212\/\u2212 mice restored the capacity to develop typical L-SAT, enhanced anti-MTg IgG1 and IgG2b production, up-regulated MHC class II expression on thyrocytes and decreased thyrocyte proliferation. These results suggest that IFN-\u03b3 plays a dual role in the development of SAT. IFN-\u03b3 is required for development of L-SAT, and it also functions to inhibit thyroid epithelial cell proliferation.<\/jats:p>","DOI":"10.4049\/jimmunol.169.7.3999","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T19:18:01Z","timestamp":1398107881000},"page":"3999-4007","source":"Crossref","is-referenced-by-count":49,"title":["Dual Roles for IFN-\u03b3, But Not for IL-4, in Spontaneous Autoimmune Thyroiditis in NOD.H-2h4 Mice"],"prefix":"10.1093","volume":"169","author":[{"given":"Shiguang","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gordon C","family":"Sharp","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"},{"name":"Department of Pathology, University of Missouri School of Medicine , Columbia, MO 65212"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Braley-Mullen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"},{"name":"Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine , Columbia, MO 65212"},{"name":"Veterans Affairs Research Service , Columbia, MO 65212"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,10,1]]},"reference":[{"key":"2026020209213828400_R1","first-page":"287","volume-title":"Clin. 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