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Posted by / 07-Jul-2016 01:17

In this regard it is of interest that persistent, apparently benign virus infection of the thyroid can be induced in mice (220), and that infection of neonatal mice with reo virus induces a polyendocrine autoimmunity (Fig. These agents could work by liberating thyroid antigens.

In theory an initial response to one antigen might proceed by reacting to the other antigen, and thereby spread and augment the autoimmune process.If so, this phenomenon would help to explain the high frequency of AITD in women.Twins from opposite sex pairs should have an increased risk of thyroid autoimmunity compared to monozygotic twins if microchimerism has a role, and indeed such twins have been found to have more frequent thyroid autoantibodies (209).For instance, in a recent study of an animal model of Graves’ disease, 5α-dihydrotestosterone was given to mice a week before immunization with TSH-R, and this reduced both the severity of the hyperthyroidism that developed and downregulated the Th1 response (211a).Another hypothetical reason for the unequal sex ratio is that skewed X chromosome inactivation could contribute through the failure of some autoantigens expressed on one X chromosome to be expressed at a critical point in the disease pathway.

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One might turn the first argument around and suggest that thyroiditis results from a lack of exposure to TG at some period, an exposure that is necessary to depress continuously an otherwise inevitable immune response.

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