Spontaneous autoimmune thyroiditis in the rat accelerated by thymectomy and low doses of irradiation: mechanisms implicated in the pathogenesis.

Factors involved in the production of autoimmune thyroiditis in thymectomized and sublethally irradiated rats were investigated. The study suggested that a gene linked to RT1 of the rat major histocompatibility complex (MHC), a selective depletion of suppressor T cells and high radiosensitivity of the thyroid gland were required in varying degrees to initiate the autoimmune thyroiditis in these rats. K cells in the spleen markedly increased at the initial stage and subsequently decreased at the appearance of the thyroid lesion, suggesting the consumption of K cells by thyroid antigen--antibody complexes formed in situ and in the circulation. Our data generally support the three genes concept proposed by Rose et al. (1976, 1980) that at least three genetically determined defects participate in triggering the production of autoimmune thyroiditis--namely, Ir genes within the MHC of the species, diminished ability of T cells to suppress autoimmune responses and a genetic defect in the thyroid gland.