SPONTANEOUS AUTOIMMUNE-THYROIDITIS IN THE RAT ACCELERATED BY THYMECTOMY AND LOW-DOSES OF IRRADIATION - MECHANISMS IMPLICATED IN THE PATHOGENESIS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 45  (2) , 329-337
Abstract
Factors involved in the production of autoimmune thyroiditis in thymectomized and sublethally irradiated rats were investigated. 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 probably were required in varying degrees to initiate the autoimmune thyroiditis in these rats. K [killer] 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. The data generally support the 3 genes concept proposed by Rose that at least 3 genetically determined defects participate in triggering the production of autoimmune thyroiditis, i.e., 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.