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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...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
Regulation of Hormone Secretion01:19

Regulation of Hormone Secretion

Regulation of hormone secretion is a finely tuned orchestration driven by various types of stimuli, encompassing neural, humoral, and hormonal signals. Environmental cues instigate neural stimuli, where action potentials traverse nerve fibers to reach their designated targets. An illustrative scenario is the body's response to stress, wherein the sympathetic nervous system releases epinephrine from the adrenal glands, inducing the well-known 'fight or flight' reaction.
Humoral stimuli,...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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: May 16, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Ingested (oral) thyrotropin releasing factor (TRH) inhibits EAE.

Staley A Brod1, Victoria Bauer

  • 1Department of Neurology, University of Texas-Houston, Health Science Center, 6431 Fannin St., Houston, TX 77030, United States. staley.a.brod@uth.tmc.edu

Cytokine
|November 15, 2012
PubMed
Summary

Oral administration of thyrotropin-releasing factor (TRH) effectively reduced inflammation and disease severity in experimental autoimmune encephalomyelitis (EAE). TRH modulated cytokine profiles, decreasing pro-inflammatory Th1 and Th17 responses while increasing anti-inflammatory Th2 cytokines.

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Area of Science:

  • Neuroimmunology
  • Inflammatory Diseases
  • Protein Therapeutics

Background:

  • Ingested immunoactive proteins can modulate autoimmune diseases like experimental autoimmune encephalomyelitis (EAE).
  • Previous studies showed that proteins like Type I IFN, SIRS peptide 1-21, α-MSH, ACTH, and SST inhibit EAE by altering cytokine profiles and T cell responses.

Purpose of the Study:

  • To investigate the potential anti-inflammatory effects of orally administered thyrotropin-releasing factor (TRH) in EAE.
  • To determine if TRH exhibits similar therapeutic benefits to other ingested immunoactive proteins in EAE models.

Main Methods:

  • C57BL/6 mice with MOG peptide 35-55 induced EAE were gavaged with TRH or saline.
  • Splenocytes from TRH-treated mice were adoptively transferred to recipient mice with ongoing EAE.
  • Cytokine levels (IL-17, TNF-α, IL-13) and clinical scores were assessed in both actively treated and recipient mice.

Main Results:

  • Oral TRH significantly inhibited ongoing EAE, reducing clinical scores and central nervous system (CNS) inflammation.
  • Adoptive transfer of cells from TRH-fed donors conferred protection against EAE in recipient mice.
  • TRH treatment decreased pro-inflammatory cytokines (IL-17, TNF-α) and increased anti-inflammatory IL-13 in the spleen and CNS, without significantly altering T(reg) cell frequencies.

Conclusions:

  • Orally administered TRH demonstrates significant therapeutic potential for EAE.
  • TRH exerts its anti-inflammatory effects by modulating Th1/Th17 and Th2 cytokine balance within the CNS.
  • TRH represents a promising candidate for oral therapy in autoimmune inflammatory conditions affecting the CNS.