Related Experiment Video

Updated: Jul 30, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Inflammatory cytokine regulation of TRAIL-mediated apoptosis in thyroid epithelial cells

J D Bretz1, E Mezosi, T J Giordano

  • 1Department of Medicine, University of Michigan Medical Center, Ann Arbor, Michigan, USA.

Cell Death and Differentiation
|February 23, 2002
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can trigger thyroid cell death when combined with inflammatory cytokines. Interferon-gamma (IFNγ) blocks this TRAIL-induced apoptosis, suggesting a complex role in autoimmune thyroiditis.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Chronic autoimmune thyroiditis involves target organ destruction.
  • Death receptor-mediated apoptosis is a key mechanism in this process.
  • Inflammatory cytokines (IL-1, TNF, IFNγ) modulate autoimmune thyroiditis.

Purpose of the Study:

  • To investigate the role of TRAIL in thyroid epithelial cell apoptosis.
  • To determine the effect of inflammatory cytokines on TRAIL-induced apoptosis.
  • To explore the in vivo relevance of TRAIL signaling in thyroid tissue.

Main Methods:

  • Primary normal thyroid epithelial cells were treated with TRAIL and combinations of IL-1β, TNFα, and IFNγ.
  • Cell surface expression of TRAIL receptors (DR4, DR5) was analyzed.
  • In vivo presence of TRAIL and its receptors (DR5, DcR1) in thyroid tissues was examined.

Main Results:

  • TRAIL induced apoptosis in thyroid cells when combined with IL-1β and TNFα.
  • IFNγ inhibited TRAIL-induced apoptosis.
  • Cytokine-mediated regulation involved changes in DR5 cell surface expression.
  • TRAIL, DR5, and DcR1 were found in both normal and inflamed thyroid tissues.

Conclusions:

  • TRAIL-mediated apoptosis may contribute to thyroid damage in autoimmune thyroiditis.
  • Inflammatory cytokines differentially regulate TRAIL signaling in thyroid cells.
  • DR5 is a key receptor in the cytokine-mediated modulation of TRAIL-induced apoptosis.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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...
Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
The exact mechanisms by which calcitonin operates in calcium homeostasis remain elusive, but its significance is evident in several vital...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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...