Читать книгу The Healthy Thyroid: What you can do to prevent and alleviate thyroid imbalance - Patsy Westcott - Страница 38

The presence of thyroid autoantibodies in your bloodstream is an important clue that there has been an immune attack on your thyroid. In fact, it was by studying Graves’ disease that scientists acquired some of the earliest clues of what was going on in autoimmunity. The chief culprit in Graves’ disease is an antibody, first discovered in the blood of Graves’ patients as long ago as 1956, dubbed ‘long-active thyroid stimulator’, or ‘LATS’, because in animals, it stimulated thyroid activity for longer than thyroid-stimulating hormone (TSH).

Later researchers identified LATS as a type of immunoglobulin G, the main antibody in the bloodstream and, because it stimulates thyroid production by locking onto the TSH receptor, they renamed it TSHR-Ab. This autoantibody is now thought to be responsible for the thyroid overactivity in Graves’ disease, and to play a key role in the development of thyroid eye disease by overstimulating certain cells that line the eye sockets.

A similar process is involved in Hashimoto’s thyroiditis except that, in this case, the rogue antibodies are directed against thyroglobulin (TG), the protein molecule in which thyroid hormone is stored, and thyroid peroxidase (TPO), a key enzyme involved in the early stages of manufacturing thyroid hormone. The autoantibodies block receptors on both TG and TPO, thereby causing underproduction of thyroid hormone.