Upon the cell surface of the apical microvilli of the thyroid acini is expressed the thyroid microsomal antigen. The thyroid acini are polarized and may be intact or semi-intact.

By understanding this structure, it is possible to visualise how common antibodies that are associated with thyroid autoimmune disease lead to complement mediated and antibody dependent cell toxicity.

Based on research studies, TSH receptor antibodies are now classified into two types. The first includes those that stimulate thyroid hormone synthesis and release (called TSI), while the second is one that mimics the role of TSH in its growth promotion role (called TGI).

In patients who have goitrous Grave’s disease and in a few with euthyroid non-toxic goitre, the presence of TGI has now identified novel thyroid autoimmunity.

In a majority with nontoxic goitre, there is a specific lack of lymphoid thyroiditis and a reduced chance of occurrence of thyroglobulin or microsomal antibodies. Instead, the autoimmunity is expressed through hyperplasia and hypertrophy of the thyroid gland itself.

While both TSI and TGI have stimulating effects, they can also have blocking effects and have been called TSI block and TGI block respectively.

In myxoedema, the thyroid gland atrophy occurs due to impaired pituitary controlled repair. This is because of high prevalence of these blocking antibodies.

However, in goitrous thyroiditis, these blocking antibodies do not exist. This leads to uninhibited TSH influence on the thyroid gland.

The presence of these antibodies can be easily confirmed in euthyroid subjects. Those who receive TSI blockers do not develop hyperthyroidism, while those who receive growth promoting antibodies eventually develop a goitre.