Humoral and cellular immune responses are both involved in autoimmune disorders of the thyroid gland. In the last five years, new substantial data have been obtained on the nature and the expression of thyroid cell surface
autoantigens and on the demonstration of the functional heterogeneity of
autoantibodies to the
thyroid stimulating hormone (
TSH) receptor. In the present report, attention will be mainly focused on recent studies carried out in our laboratory. The main
autoantigens so far identified include the 'microsomal'
antigen,
thyroglobulin and the
TSH receptor. For many years the 'microsomal'
antigen (M) was considered a poorly characterized constituent of the cytoplasm of the thyroid cell. In the last five years, several lines of evidence were provided indicating that M is also well represented on the surface of the follicular cell and is identical to
thyroid peroxidase (TPO). The use of anti-TPO
monoclonal antibodies, presently available, have confirmed this antigenic identity. Microsomal (anti-TPO)
antibodies are very useful markers of autoimmune thyroid disorders and are generally present in Hashimoto's
thyroiditis, idiopathic
myxedema and
Graves' disease.
TSH receptor antibodies (TRAb) are present in the sera of patients with
Graves' disease. TRAb are able to stimulate thyroid
adenylate cyclase and also to mimic TSH in its thyroid growth stimulation. Thus, these
antibodies may have a pathogenetic role in
goiter formation and in thyroid hyperfunction in
Graves' disease. TRAb were also shown to inhibit both TSH binding to its receptor and TSH-stimulated
adenylate cyclase activity. Recently TRAb, which inhibited TSH-stimulated
adenylate cyclase activity, were found in idiopathic
myxedema patients and may be responsible for impairment of thyroid function.(ABSTRACT TRUNCATED AT 250 WORDS)