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I was reading about Graves' disease, which is an autoimmune disorder. I read a few books, including Endocrinology by Hadley and Levine, and websites where they mentioned that the antibody named TSAb (Thyroid stimulating Antibody) binds to TSH receptors and stimulates synthesis and release of thyroid hormones from thyroid gland. This results in the symptoms of Exopthalmic goiter or Graves' disease.

My question is how are these antibodies actually attacking the healthy tissues (which I presume is the tissue of thyroid gland)?

I've so far found no website explaining this part of the autoimmune disorder. I'd appreciate any information or references in this regard.

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Thyroid stimulating antibodies (sTRAb) don't destroy thyroid tissue. To the contrary, they have a TSH-like effect on thyrocytes and therefore lead to hyperthyroidism and thyroid growth resulting in goiter. The exception is Graves' disease with Hashimoto component. Here, the thyroid is also affected by cytotoxic T cells and antibodies directed against thyroid peroxidase, which gives rise to destruction of the thyroid. But even in this case, it aren't the sTRAb, which destroy tissue.

Perhaps healthy tissues refers to extrathyroidal tissues. Due to unknown reasons several tissues including skeletal muscle, heart muscle, adipose tissue and skin have TSH receptors, and they are affected by sTRAb, too. Hypertrophy results from cross-talk of TSH receptors with IGF-1 receptors in Graves' disease.

References

  1. Dietrich JW, Landgrafe G, Fotiadou EH. TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis. J Thyroid Res. 2012;2012:351864. doi: 10.1155/2012/351864. Epub 2012 Dec 30. PMID 23365787.

  2. Krieger CC, Neumann S, Place RF, Marcus-Samuels B, Gershengorn MC. Bidirectional TSH and IGF-1 receptor cross talk mediates stimulation of hyaluronan secretion by Graves' disease immunoglobins. J Clin Endocrinol Metab. 2015 Mar;100(3):1071-7. doi: 10.1210/jc.2014-3566. Epub 2014 Dec 8. PMID 25485727.

  3. Krieger CC, Place RF, Bevilacqua C, Marcus-Samuels B, Abel BS, Skarulis MC, Kahaly GJ, Neumann S, Gershengorn MC. TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis. J Clin Endocrinol Metab. 2016 Jun;101(6):2340-7. doi: 10.1210/jc.2016-1315. PMID 27043163.

  4. Yoo WS, Chung HK. Recent Advances in Autoimmune Thyroid Diseases. Endocrinol Metab (Seoul). 2016 Aug 26. PMID 27586448.

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In an autoimmune disorder body tissues are not necessarily damaged, the immune system can also cause

  • Altered organ growth
  • Altered organ function

Grave's disease is a result of altered organ function causing hyperthyroidism due to hypersensitivity reaction.

It is hypersensitivity Type-V.

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Wikipedia: Hypersensitivity

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