Document Detail


The role of stress in the clinical expression of thyroid autoimmunity.
MedLine Citation:
PMID:  17192582     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During stress, activation of the hypothalamic-pituitary-adrenal 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-presenting 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-mediated immune activity may promote apoptotic pathways on thyroid follicular cells leading to thyroid cell destruction and HT. Conversely, predominance of Th2-mediated immune response may induce antigen-specific B lymphocytes to produce anti-TSH receptor (TSHr) antibodies causing GD. The weight of evidence from epidemiological and case-control 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-Th2 balance away for Th1 and toward Th2. Conversely, recovery from stress or the immune suppressive effect of pregnancy may induce a Th2 to Th1 "return shift" leading to autoimmune (sporadic) or postpartum thyroiditis, respectively.
Authors:
Agathocles Tsatsoulis
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1088     ISSN:  0077-8923     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-12-28     Completed Date:  2007-03-05     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  382-95     Citation Subset:  IM    
Affiliation:
Department of Endocrinology, University of Ioannina, 45110, Ioannina, Greece. atsatsou@cc.uoi.gr
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MeSH Terms
Descriptor/Qualifier:
Animals
Autoimmunity / physiology
Graves Disease / immunology*
Humans
Neuroimmunomodulation / immunology
Neurosecretory Systems / immunology*
Stress, Physiological / immunology*
Thyroid Gland / immunology*

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