{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T01:10:06Z","timestamp":1773277806290,"version":"3.50.1"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Transgenic NOD.H-2h4 mice expressing TGF-\u03b2 under control of the thyroglobulin promoter were generated to assess the role of TGF-\u03b2 in the development of thyrocyte hyperplasia. In contrast to nontransgenic littermates, which develop lymphocytic spontaneous autoimmune thyroiditis (L-SAT), all TGF-\u03b2 transgenic (Tg) mice given NaI water for 2\u20137 mo developed thyroid lesions characterized by severe thyroid epithelial cell hyperplasia and proliferation, with fibrosis and less lymphocyte infiltration than in nontransgenic mice. Most Tg mice produced less anti-mouse thyroglobulin autoantibody than did wild type (WT) mice. T cells from Tg and WT mice were equivalent in their ability to induce L-SAT after transfer to SCID or TCR\u03b1\u2212\/\u2212 mice. WT lymphocytes could transfer experimental autoimmune thyroiditis or L-SAT to Tg mice, indicating that the transgenic environment did not prevent migration of lymphocytes to the thyroid. Thyroids of Tg mice had higher frequencies of Foxp3+ regulatory T cells (Tregs) compared with nontransgenic WT mice. Transient depletion of Tregs by anti-CD25 resulted in increased infiltration of inflammatory cells into thyroids of transgenic mice. Treg depletion also resulted in increased anti-mouse thyroglobulin autoantibody responses and increased expression of IFN-\u03b3 and IFN-\u03b3\u2013inducible chemokines in thyroids of Tg mice. The results suggest that spontaneous autoimmune thyroiditis is inhibited in mice expressing transgenic TGF-\u03b2 on thyrocytes, at least in part, because there is an increased frequency of Tregs in their thyroids.<\/jats:p>","DOI":"10.4049\/jimmunol.0903620","type":"journal-article","created":{"date-parts":[[2010,3,25]],"date-time":"2010-03-25T03:44:58Z","timestamp":1269488698000},"page":"5352-5359","source":"Crossref","is-referenced-by-count":17,"title":["Transgenic Expression of TGF-\u03b2 on Thyrocytes Inhibits Development of Spontaneous Autoimmune Thyroiditis and Increases Regulatory T Cells in Thyroids of NOD.H-2h4 Mice"],"prefix":"10.1093","volume":"184","author":[{"given":"Shiguang","family":"Yu","sequence":"first","affiliation":[{"name":"*Research Service, Department of Veterans Affairs;"},{"name":"\u2020Department of Internal Medicine,"},{"name":"\u2021Department of Biological Science, Arkansas Biosciences Institute, Arkansas State University, Jonesboro, AR 72467"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yujiang","family":"Fang","sequence":"additional","affiliation":[{"name":"*Research Service, Department of Veterans Affairs;"},{"name":"\u2020Department of Internal Medicine,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gordon C.","family":"Sharp","sequence":"additional","affiliation":[{"name":"\u2020Department of Internal Medicine,"},{"name":"\u00a7Department of Pathology, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helen","family":"Braley-Mullen","sequence":"additional","affiliation":[{"name":"*Research Service, Department of Veterans Affairs;"},{"name":"\u2020Department of Internal Medicine,"},{"name":"\u00b6Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212; and"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2010,5,1]]},"reference":[{"key":"2023010203025623200_r1","doi-asserted-by":"crossref","first-page":"1286","DOI":"10.1056\/NEJM199411103311907","article-title":"Transforming growth factor beta in tissue fibrosis.","volume":"331","author":"Border","year":"1994","journal-title":"N. 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