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Synthesis and Regulation of Thyroid Hormones

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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.
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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...

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Hypothyroidism II: Pathophysiology

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Related Experiment Video

Updated: Jun 5, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Thyroperoxidase, thyroglobulin, Na(+)/I(-) symporter, pendrin in thyroid autoimmunity.

Barbara Czarnocka¹

¹Department of Biochemistry and Molecular Biology, Medical Center of Postgraduate Education, 99/103 Marymoncka Street, 01-813 Warsaw, Poland. barbarac@cmkp.edu.pl

Frontiers in Bioscience (Landmark Edition)

|January 4, 2011

Summary

Autoimmune thyroid diseases involve antibodies attacking thyroid proteins like thyroperoxidase and thyroglobulin. This review details the function and immune response to these and newer antigens, Na+/I- symporter and pendrin.

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Last Updated: Jun 5, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Published on: March 17, 2023

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Area of Science:

Endocrinology
Immunology
Molecular Biology

Background:

Autoimmune thyroid diseases (AITD), including Graves' disease and Hashimoto's thyroiditis, are common endocrine disorders.
These conditions involve lymphocytic infiltration and autoantibody production against thyroid-specific proteins.
Key autoantigens include thyroperoxidase (TPO), thyroglobulin (Tg), and the thyrotropin hormone receptor.

Purpose of the Study:

To review the current understanding of the pathophysiology and immunogenic responses to TPO, Tg, Na+/I- symporter (NIS), and pendrin.
To elucidate the molecular mechanisms underlying autoimmune thyroid diseases.
To highlight the roles of novel autoantigens in AITD.

Main Methods:

Literature review of existing research on thyroid autoantigens.
Analysis of the physiological functions of TPO, Tg, NIS, and pendrin.
Examination of the immune system's response to these proteins in AITD.

Main Results:

TPO and Tg autoantibodies are established hallmarks of AITD.
Na+/I- symporter (NIS) and pendrin are identified as novel autoantigens in AITD.
The clinical and pathological significance of NIS and pendrin autoantibodies requires further investigation.

Conclusions:

Understanding the autoantigens is crucial for deciphering AITD pathogenesis.
Further characterization of NIS and pendrin autoantibodies is needed.
This review consolidates knowledge on key proteins involved in autoimmune thyroid disease.