TRAb's are subdivided into activating, blocking and neutral antibodies, depending on their effect on the TSH receptor.
Graves' disease and Hashimoto's thyroiditis are commonly associated with the presence of anti-thyroid autoantibodies.
Anti-thyroid peroxidase (anti-TPO) antibodies are specific for the autoantigen TPO, a 105 kDa glycoprotein that catalyses iodine oxidation and thyroglobulin tyrosyl iodination reactions in the thyroid gland.
[4][6][7] High serum antibodies are found in active phase chronic autoimmune thyroiditis.
[4][7][8] The majority of anti-TPO antibodies are produced by thyroid infiltrating lymphocytes, with minor contributions from lymph nodes and the bone marrow.
It is a seven transmembrane G protein-coupled receptor that is involved in thyroid hormone signalling.
Although the exact mechanism of how TRAbs induce Graves' ophthalmopathy is unknown, it is likely that the antibodies bind to TSH receptors in retro-orbital tissues, causing infiltration of lymphocytes.
[1] The production of antibodies in Graves' disease is thought to arise by activation of CD4+ T-cells, followed by B-cell recruitment into the thyroid.
[16] In 1912 Hakaru Hashimoto described hypothyroidism and goiter associated with thyroid lymphoid infiltration.
In 1956 the anti-Tg antibody was detected in similar cases, elucidating the autoimmune cause of these characteristics.