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TNF-\u03b1 is an important proinflammatory cytokine and apoptotic molecule involved in many autoimmune diseases. To study its role in G-EAT, anti-TNF-\u03b1 mAb was given to recipient mice. Disease severity was comparable between mice with or without anti-TNF-\u03b1 treatment at days 19\u201321, the time of maximal severity of G-EAT, suggesting TNF-\u03b1 is not essential for development of thyroid inflammation. However, thyroid lesions resolved at day 48 in anti-TNF-\u03b1-treated mice, while thyroids of rat Ig-treated controls had fibrosis. These results suggested that reducing TNF-\u03b1 contributed to resolution of inflammation and inhibited fibrosis. Gene and protein expression of inflammatory molecules was examined by RT-PCR and immunostaining, and apoptosis was detected using TUNEL staining and an apoptosis kit. Thyroids of anti-TNF-\u03b1-treated controls had reduced proinflammatory and profibrotic molecules, e.g., IFN-\u03b3, IL-1\u03b2, IL-17, inducible NOS and MCP-1, at day 19 compared with thyroids of rat Ig-treated mice. There were more apoptotic thyrocytes in rat Ig-treated controls than in anti-TNF-\u03b1-treated mice. The site of expression of the anti-apoptotic molecule FLIP also differed between rat Ig-treated and anti-TNF-\u03b1-treated mice. FLIP was predominantly expressed by inflammatory cells of rat Ig-treated mice and by thyrocytes of anti-TNF-\u03b1-treated mice. These results suggest that anti-TNF-\u03b1 may regulate expression of proinflammatory cytokines and apoptosis in thyroids, resulting in less inflammation, earlier resolution, and reduced fibrosis.<\/jats:p>","DOI":"10.1189\/jlb.0606402","type":"journal-article","created":{"date-parts":[[2006,10,18]],"date-time":"2006-10-18T02:59:14Z","timestamp":1161140354000},"page":"306-314","source":"Crossref","is-referenced-by-count":57,"title":["Decreasing TNF-\u03b1 results in less fibrosis and earlier resolution of granulomatous experimental autoimmune thyroiditis"],"prefix":"10.1093","volume":"81","author":[{"given":"Kemin","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Missouri School of Medicine , Columbia, Missouri , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongzhong","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Missouri School of Medicine , Columbia, Missouri , USA"}],"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, Missouri , USA"},{"name":"Department of Pathology, University of Missouri School of Medicine , Columbia, Missouri , USA"}],"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, Missouri , USA"},{"name":"Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine , Columbia, Missouri , USA"},{"name":"VA Research Service , Columbia, Missouri , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,10,17]]},"reference":[{"key":"2023033007420245000_","doi-asserted-by":"crossref","first-page":"299","DOI":"10.1111\/j.1600-065X.1981.tb00346.x","article-title":"T-cell regulation in autoimmune thyroiditis","volume":"55","author":"Rose","year":"1981","journal-title":"Immunol. 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