Immunological aspects of autoimmune thyroid disease.
There is considerable evidence to indicate that autoimmune thyroid diseases (both Graves disease and Hashimoto thyroiditis) are primary disorders of the lymphoid system. Evidence is now available to indicate that both cell-mediated and humoral immune factors are important in the pathophysiological expression of these conditions. The basic genetic defect in these disorders now appears to be the presence of a specific defect in suppressor T lymphocytes, which in turn permits the survival and expansion of a randomly appearing "forbidden" clone of thyroid-directed, organ-specific, helper T lymphocytes. These then cooperate with already present groups of appropriate B lymphocytes, which in turn produce humoral immunoglobulins directed against the thyroid. There appear to be subtle genetic differences that distinguish between Graves disease and Hashimoto thyroiditis, leading to their different expressions. Indeed, subtle genetic differences between different groups of patients with Graves disease may reveal whether there is a complete defect in immunoregulation (thus preventing any immunological remission) or a partial defect in immunoregulation, in which case the possibility of remission does exist. The role of stress in precipitating hyperthyroidism may be via stress-related physiological effects on partially defective suppressor T lymphocytes.
D000917:Antibody Formation; D000941:Antigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology*; D005128:Eye Diseases / Q000276:immunology; D006111:Graves Disease / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000502:physiology; D013312:Stress, Physiological / Q000150:complications; D013959:Thyroid Diseases / Q000235:genetics / Q000276:immunology*; D013967:Thyroiditis, Autoimmune / Q000276:immunology
D000941:Antigens; D007136:Immunoglobulins