Thyroid antibodies in thyroid diseases.

Abstract

The cell surface expression of the thyroid microsomal antigen is confined to the apical microvilli of the polarized cells in intact or semi-intact thyroid acini. This makes it possible to envisage a pathogenetic role for the commonest antibodies found in thyroid autoimmunity by mechanisms involving complement- and antibody-dependent cytotoxicity. TSH rereceptor antibodies can now be differentiated into those that stimulate hormone synthesis and release (TSI), and those which mimic TSH in its growth-promoting function (TGI). TGI were demonstrated in goitrous Graves' disease and in some patients with euthyroid non-toxic goitres, diffuse or nodular, defining a new variety of thyroid autoimmunity. In patients with non-toxic goitre there is hardly any lymphoid thyroiditis and a low incidence of thyroglobulin or microsomal antibodies, the main expression of autoimmunity being the impetus to thyroid hyperplasia and hypertrophy. TSH receptor antibodies of both types, TSI and TGI, can either be stimulating or have blocking effects (TSI block and TGI block). Atrophy of the thyroid gland in myxoedema is due to blocking of the normal pituitary-controlled repair mechanism. In goitrous thyroiditis cell re-growth as a result of increased TSH can occur, as there are no blocking antibodies. In some patients with 'simple' euthyroid goitres, TSI blockers prevent the onset of hyperthyroidism while growth-promoting antibodies give rise to the goitre.