Immune-endocrine interactions in autoimmune thyroid diseases

KLECHA AJ; BARREIRO ARCOS ML; FRICK LR; GENARO AM; CREMASCHI G

NEUROIMMUNOMODULATION.

S. Karger Medical and Scientific Publishers

Año: 2008 vol. 15 p. 68 - 75

1021-7401

Autoimmune thyroid diseases (AITD) are the most common organ specific autoimmune disorders affecting approximately 5% of the overall population. An aberrant interaction between abnormal thyrocytes, abnormal antigen-presenting cells (APC) and abnormal T cells forms the basis for the atypical autoimmune reaction targeting thyroid antigens. It was proposed that non-genetic (environmental and  hormonal) factors play a crucial etiologic role in AITD development, through altering immune-endocrine interactions. The most outstanding fact is that in genetically susceptible (predisposed) individuals the disruption of these neuroendocrine-immune interactions by  enviromental factors result in the outcome of thyroid autoimmune dysfunction. These interactions are able to incline the balance between Th1-Th2 immune response toward one side, resulting in a Th1-cell-mediated autoimmune reaction with thyrocyte destruction and hypothyroidism in Hashimoto’s thyroiditis (HT) but to an hyperreactive Th2-mediated humoral response against TSH-R with stimulatory antibodies leading to Graves’ disease (GD) hypertiroidism. In this review a picture of the main mechanisms involved are summarized. In this sense, the participation of stress-mediated activation of SA and HPA axis, the hormonal changes occuring during pregnancy and post-partum acting on APC and  influencing, in this way, the balance of immune status are shown to participate in AITD etiology. The possibility that altered levels of thyroid hormones during the course of the AITD may alter immune function is also discussed.