H‐2 gene products influence susceptibility of target thyroid gland to damage in experimental autoimmune thyroiditis

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Abstract
The restriction of the pathogenesis of experimental autoimmune thyroiditis (EAT) by H‐2 gene products was investigated. EAT was induced by injecting thyroglobulin extract plus adjuvant into F1, hybrid mice that had been implanted under the kidney capsules with thyroid glands originating from either the EAT‐susceptible or ‐resistant parental strain mice. We found relative H‐2 restriction of thyroid damage to those glands originating from the H‐2‐susceptible parental strain. H‐2 restriction of damage at the level of the target thyroid gland implicates cytotoxic effector T lymphocytes as a pathogenic agent of EAT.