RESUMO
Autoimmune thyroid disease (AITD) shows the highest incidence among organ-specific autoimmune diseases and is the most common thyroid disease in humans, including Graves' disease (GD) and Hashimoto's thyroiditis (HT). The susceptibility to autoimmune diseases is affected by increased autoantibody levels, susceptibility gene polymorphisms, environmental factors, and psychological factors, but the pathogenesis remains unclear. Various cytokines and related genes encoding them play important roles in the development and progression of AITD. CD152, an expression product of the CTLA-4 gene, downregulates T cell activation. The A/A genotype polymorphism in the CT60 locus may reduce the production of thyroid autoantibodies. The C1858T polymorphism of the PTNP22 gene reduces the expression of its encoded LYP, which increases the risk of GD and HT. GD is an organ-specific autoimmune disease involving increased secretion of thyroid hormone, whereas HT may be associated with the destruction of thyroid gland tissue and hypothyroidism. These two diseases exhibit similar pathogenesis but opposite trends in the clinical manifestations. In this review, we focus on the structure and function of these cytokines and related genes in AITD, as well as the association of polymorphisms with susceptibility to GD and HT, and attempt to describe their differences in pathogenesis and clinical manifestations.
Assuntos
Doenças Autoimunes/genética , Doenças Autoimunes/metabolismo , Polimorfismo Genético/genética , Doenças da Glândula Tireoide/genética , Doenças da Glândula Tireoide/metabolismo , Animais , Antígeno CTLA-4/genética , Predisposição Genética para Doença/genética , Doença de Graves/genética , Doença de Graves/metabolismo , Doença de Hashimoto/genética , Doença de Hashimoto/metabolismo , HumanosRESUMO
Sulfur mustard [bis (2-chloroethyl) sulfide, sulfur mustard, SM] is considered a powerful chemical warfare agent.There is still no specific antidote due to its complex toxicological mechanism .An intimate knowledge of the toxic mechanisms and pathophysiological changes is important to the treatment of sulfur mustard injury .Oxidative stress is one of the most important pathophysiological processes involved in the toxic effect of sulfur mustard .The study of oxidative stress biomarkers induced by sulfur mustard can help to reveal the role of oxidative stress in sulfur mustard intoxication , which may contribute to better understanding of the toxic mechanism and development of therapeutic measures after sulfur mustard exposure.The research advances in oxidative stress biomarkers in sulfur mustard intoxication are reviewed .