{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T01:36:06Z","timestamp":1778636166982,"version":"3.51.4"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2001,12,1]],"date-time":"2001-12-01T00:00:00Z","timestamp":1007164800000},"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":[[2001,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Nearly 100% of NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and produce anti-mouse thyroglobulin autoantibodies when they receive 0.05% NaI in their drinking water beginning at 8 wk of age. Our previous studies showed that TGF\u03b21 mRNA was constitutively expressed in thyroids and spleens of normal NOD.H-2h4 mice but not other strains of mice. To determine whether TGF\u03b2 might have a role in SAT, mice were given anti-TGF\u03b2 mAb at various times during development of SAT. Anti-TGF\u03b2 markedly inhibited development of SAT and production of anti-mouse thyroglobulin IgG1 autoantibodies. Anti-TGF\u03b2 was most effective in inhibiting SAT when given during the time thyroid lesions were developing, i.e., starting 4 wk after administration of NaI water. The active form of the TGF\u03b21 protein was present in thyroids of mice with SAT but not in normal NOD.H-2h4 thyroids. However, thyrocytes of normal NOD.H-2h4 thyroids did express latent TGF\u03b21. TGF\u03b21 protein expression in the thyroid correlated with SAT severity scores, and administration of anti-TGF\u03b2 inhibited TGF\u03b21 protein expression in both the thyroid and spleen. TGF\u03b21 was produced primarily by inflammatory cells and was primarily localized in areas of the thyroid containing clusters of CD4+ T and B cells. Depletion of CD8+ T cells had no effect on TGF\u03b21 protein expression. Activation of splenic T cells was apparently not inhibited by anti-TGF\u03b2, because up-regulation of mRNA for cytokines and other T cell activation markers was similar for control and anti-TGF\u03b2-treated mice. TGF\u03b21 may function by promoting migration to, or retention of, inflammatory cells in the thyroid.<\/jats:p>","DOI":"10.4049\/jimmunol.167.12.7111","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T21:31:04Z","timestamp":1398029464000},"page":"7111-7118","source":"Crossref","is-referenced-by-count":21,"title":["Role of TGF\u03b2 in Development of Spontaneous Autoimmune Thyroiditis in NOD.H-2h4 Mice"],"prefix":"10.1093","volume":"167","author":[{"given":"Helen","family":"Braley-Mullen","sequence":"first","affiliation":[{"name":"Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"},{"name":"Medical Microbiology and Immunology, University of Missouri School of Medicine , Columbia, MO 65212"},{"name":"Department of Veterans Affairs Research Service , Columbia, MO 65212"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kemin","family":"Chen","sequence":"additional","affiliation":[{"name":"Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongzhong","family":"Wei","sequence":"additional","affiliation":[{"name":"Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shiguang","family":"Yu","sequence":"additional","affiliation":[{"name":"Internal Medicine, University of Missouri School of Medicine , Columbia, MO 65212"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2001,12,15]]},"reference":[{"key":"2026020208070922700_R1","first-page":"263","volume-title":"Adv. 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