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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Related Experiment Video

Updated: Jul 11, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

TSH receptor antibodies.

Bernard Rees Smith1, Jane Sanders, Jadwiga Furmaniak

  • 1FIRS Laboratories, RSR Ltd., Parc Ty Glas, Llanishen, Cardiff, United Kingdom. firs@rsrltd.eclipse.co.uk

Thyroid : Official Journal of the American Thyroid Association
|September 29, 2007
PubMed
Summary
This summary is machine-generated.

Thyroid-stimulating autoantibodies target the thyroid-stimulating hormone receptor (TSHR). Monoclonal antibodies (MAbs) like M22 and 5C9 offer insights into TSHR autoimmunity and potential therapeutic strategies for thyroid disorders.

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Area of Science:

  • Endocrinology
  • Immunology
  • Structural Biology

Background:

  • Thyroid-stimulating autoantibodies, discovered 50 years ago, are crucial in thyroidology.
  • The thyroid-stimulating hormone receptor (TSHR) is the key antigen for these autoantibodies.
  • Advancements include cloning the TSHR and developing monoclonal antibodies (MAbs).

Purpose of the Study:

  • To review the historical discovery and characterization of thyroid-stimulating autoantibodies.
  • To highlight the significance of monoclonal antibodies (MAbs) in understanding TSHR autoimmunity.
  • To discuss the potential of MAbs for diagnostic assays and therapeutic interventions.

Main Methods:

  • Characterization of mouse and human MAbs against TSHR.
  • Determination of the crystal structure of the TSHR leucine-rich domain in complex with M22.
  • Isolation and planned molecular-level studies of blocking-type MAbs like 5C9.

Main Results:

  • Mouse and human MAbs (M22) with strong thyroid-stimulating activity have been generated.
  • The crystal structure revealed M22 mimics TSH binding to TSHR.
  • A blocking-type MAb (5C9) was isolated, offering insights into differential antibody functions.

Conclusions:

  • MAbs have significantly advanced the understanding of TSHR and TSHR autoimmunity.
  • M22-TSHR structural data enables rational drug design for TSHR-autoantibody interactions.
  • Blocking MAbs like 5C9 hold therapeutic potential for inhibiting TSHR stimulation.