pathogenesis

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The basic defect in Hashimoto's disease appears to be a deficiency of antigen-specific suppressor T cells. This permits uncontrolled attack on the follicular cells by cytotoxic T cells with simultaneous unregulated T helper cell participation in the formation of autoantibodies by B-cells.

The autoantibodies most consistently found in Hashimoto's disease are to the TSH receptor and to thyroid microsomes. Those to the TSH receptor are thyroid growth stimulating immunoglobulins. Less commonly, there are autoantibodies to thyroglobulin and to follicular cell membranes.

Thyroid enlargement probably reflects:

  • thyroid growth without increased hormone synthesis
  • lymphocytic infiltration
  • occasionally, increased TSH levels

The thyroglobulin and thyroid microsomal antibodies are probably secondary to follicular cell damage initiated by cytotoxic T cells.

The association with the HLA-DR5 genotype may indicate a genetic predisposition to this pattern of autoantibody production.

Last reviewed 01/2018

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