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Related Concept Videos

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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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Related Experiment Video

Updated: Jun 22, 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 - autoantibody interactions.

B Rees Smith1, J Sanders, M Evans

  • 1FIRS Laboratories, RSR Ltd, Cardiff , UK. firs@rsrltd.eclipse.co.uk

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|June 17, 2009
PubMed
Summary
This summary is machine-generated.

Thyroid-stimulating hormone receptor (TSHR) autoantibodies (TRAbs) can stimulate or block TSHR function. This study proves a single patient can produce both stimulating and blocking TRAbs simultaneously, offering new insights into TSHR autoimmunity.

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High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model
11:31

High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model

Published on: August 16, 2019

Area of Science:

  • Endocrinology
  • Immunology
  • Molecular Biology

Background:

  • Thyroid-stimulating hormone receptor (TSHR) autoantibodies (TRAbs) play a critical role in TSHR autoimmunity, exhibiting either stimulating or blocking activity.
  • The molecular mimicry between TSHR autoantibodies and TSH has been observed, but the evolutionary basis remains unclear.
  • Previous studies suggested distinct binding sites for stimulating and blocking TRAbs on the TSHR.

Purpose of the Study:

  • To investigate the simultaneous production of both stimulating and blocking TRAbs in a single patient.
  • To analyze the binding characteristics of different TRAbs to the TSHR.
  • To provide evidence for the co-existence of TRAbs with opposing functions.

Main Methods:

  • Isolation and characterization of human monoclonal TRAbs (M22, 5C9, K1-18, K1-70) with stimulating and blocking activities.
  • Analysis of V region genes to determine the origin of isolated antibodies.
  • Binding studies of TRAbs to TSHR fragments.

Main Results:

  • Successful isolation of stimulating (M22, K1-18) and blocking (5C9, K1-70) human monoclonal TRAbs.
  • Demonstration that a single patient can produce both stimulating and blocking TRAbs concurrently, originating from different lymphocytes.
  • Evidence that both stimulating and blocking TRAbs bind to the N-terminal region (amino acids 22-260) of the TSHR.

Conclusions:

  • A patient can simultaneously produce both stimulating and blocking TRAbs against the TSHR.
  • The findings challenge the notion of strictly separate binding domains for stimulating and blocking TRAbs.
  • Further research is needed to fully elucidate the interaction sites and mechanisms of TRAb action on the TSHR.