Liping Wu

A Study on Neonatal Tolerance Against Graves' Disease in BALB/c Mice

IntroductIon Autoimmunity is defined as, a condition characterized by a specific humoral or cell‐mediated immune response against the constituents of the body’s own tissues (autoantigens). In numerous autoimmune diseases, such an immune response is well recognized that causes damage to the self‐constituents of body tissues by the products of the immune system. Graves’ hyperthyroidism occurs after the loss of tolerance to the thyroid stimulating hormone receptor (TSHR) and the generation of thyroid stimulatory antibodies that mimic the action of thyroid‐stimulating hormone (TSH).[1]

Role of Selenium Intake for Risk and Development of Hyperthyroidism.

Purpose To investigate the importance of dietary selenium (Se) for hyperthyroidism. Methods We performed a more in-depth analysis of a large cross-sectional study of 6152 participants from two counties within the Shaanxi Province, China. These counties are characterized by different habitual Se intake. We investigated the effects of a different dietary Se supply (0.02, 0.18, 0.6, or 2.0 ppm Se) on disease development in a mouse model of Graves disease (GD). Results The cross-sectional study revealed a comparable prevalence of hyperthyroidism, irrespective of Se intake, in both counties. However, an unexpected sex-specific difference was noted, and Se deficiency might constitute a risk factor for hyperthyroidism, especially in males. In a mouse model, pathological thyroid morphology was affected, and greater Se intake exerted some protecting effects on the pathological distortion. Circulating thyroid hormone levels, malondialdehyde concentrations, total antioxidant capacity, and the titer of GD-causing TSH receptor autoantibodies were not affected by Se. Expression analysis of the transcripts in the spleen indicated regulatory effects on genes implicated in the immune response, erythropoiesis, and oxygen status. However, the humoral immune response, including the CD4/CD8 or T-helper 1/T-helper 2 cell ratio and the concentration of regulatory T cells, was similar between the experimental groups, despite the difference in Se intake. Conclusions Our data have highlighted a sexual dimorphism for the interaction of Se and thyroid disease risk in humans, with indications of a local protective effects of Se on thyroid gland integrity, which appears not to be reflected in the circulating biomarkers tested.