{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T04:27:53Z","timestamp":1792124873663,"version":"4.4.0"},"reference-count":60,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,12,8]],"date-time":"2006-12-08T00:00:00Z","timestamp":1165536000000},"content-version":"vor","delay-in-days":37,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:p><jats:bold><jats:sc>Abstract:\u2002<\/jats:sc><\/jats:bold>  <jats:bold>During stress, activation of the hypothalamic\u2010pituitary\u2010adrenal axis and the sympathoadrenal system leads to increased secretion of glucocorticoids and catecholamines, respectively, in order to maintain homeostasis. Recent evidence suggests that stress hormones, acting on antigen\u2010presenting immune cells, may influence the differentiation of bipotential T helper (Th) cells away from Th1 and toward a Th2 phenotype. This results in suppression of cellular immunity and potentiation of humoral immunity. Thyroid autoimmunity is clinically expressed as Hashimoto's thyroiditis (HT) and its variants (sporadic or postpartum thyroiditis) or as Grave's disease (GD). The different phenotypic expression of thyroid autoimmunity is largely dependent on the balance of Th1 versus Th2 immune response. A predominantly Th1\u2010mediated immune activity may promote apoptotic pathways on thyroid follicular cells leading to thyroid cell destruction and HT. Conversely, predominance of Th2\u2010mediated immune response may induce antigen\u2010specific B lymphocytes to produce anti\u2010TSH receptor (TSHr) antibodies causing GD. The weight of evidence from epidemiological and case\u2013control studies supports an association between stress and GD. On the other hand, there is little information available on the effect of stress on HT, but there is evidence for an increase in postpartum thyroiditis, following the cellular immune suppressive effect of pregnancy. Whether stress has a causative effect on GD remains elusive. Circumstantial evidence supports the hypothesis that stress may influence the clinical expression of thyroid autoimmunity in susceptible individuals favoring the development of GD by shifting the Th1\u2013Th2 balance away for Th1 and toward Th2. Conversely, recovery from stress or the immune suppressive effect of pregnancy may induce a Th2 to Th1 \u201creturn shift\u201d leading to autoimmune (sporadic) or postpartum thyroiditis, respectively.<\/jats:bold> <\/jats:p>","DOI":"10.1196\/annals.1366.015","type":"journal-article","created":{"date-parts":[[2006,12,27]],"date-time":"2006-12-27T23:33:25Z","timestamp":1167262405000},"page":"382-395","source":"Crossref","is-referenced-by-count":64,"title":["The Role of Stress in the Clinical Expression of Thyroid Autoimmunity"],"prefix":"10.1111","volume":"1088","author":[{"given":"AGATHOCLES","family":"TSATSOULIS","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,12,8]]},"reference":[{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1998.tb09006.x"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(99)00188-5"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1053\/beem.1999.0044"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.2004.02085.x"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.2004.01978.x"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(96)80606-2"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/383787a0"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5258.50"},{"key":"e_1_2_8_10_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.13.040195.001343"},{"key":"e_1_2_8_11_2","first-page":"374","article-title":"Modulatory effects of glucocorticoids and catecholamines on human interleukin\u201012 and interleukin\u201010 production: clinical implications","volume":"108","author":"Elenkov I.J.","year":"1996","journal-title":"Proc. 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