Abstract
GENES in the major histocompatibility complex (MHC) have been found to be associated with the development of autoimmune diseases, including spontaneous diseases in man1,2 and spontaneous3 or experimentally induced autoimmunity in animals4. Experimental autoimmune thyroiditis (EAT) can be induced in susceptible strains of mice, such as those with the MHC H–2k haplotype, by injecting them with mouse thyroglobulin together with complete Freund's adjuvant5. In contrast, injection of mice homozygous for the H–2b haplotype fails to induce the mononuclear cell infiltration of the thyroid gland characteristic of EAT. We report here that susceptibility to induction of EAT results from an apparent point mutation which evidently occurred at the H–2K locus of the resistant H–2b haplotype. This indicates that the H–2K glycoprotein can serve to regulate the autoimmune response to thyroglobulin.
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MARON, R., COHEN, I. Mutation at H–2K locus influences susceptibility to autoimmune thyroiditis. Nature 279, 715–716 (1979). https://doi.org/10.1038/279715a0
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DOI: https://doi.org/10.1038/279715a0
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