Related Experiment Video
Updated: May 8, 2026
05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
CXCL8 in thyroid disease: from basic notions to potential applications in clinical practice
Mario Rotondi1, Francesca Coperchini, Luca Chiovato
1Unit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri I.R.C.C.S., Laboratory for Endocrine Disruptors and Chair of Endocrinology University of Pavia, Italy.
Cytokine & Growth Factor Reviews
|September 10, 2013
Summary
Chemokine CXCL8 (interleukin-8) is implicated in thyroid homeostasis and cancer. While its role in autoimmune thyroid disease is unclear, evidence suggests CXCL8 promotes thyroid cancer growth and may indicate aggressiveness.
Area of Science:
- Endocrinology
- Oncology
- Immunology
Background:
- Chemokine CXCL8 (interleukin-8) is secreted by thyrocytes and implicated in thyroid homeostasis.
- Its precise role in thyroid diseases, including autoimmune thyroid disease and thyroid cancer, remains under investigation.
- Conflicting clinical data exist regarding serum CXCL8 levels in autoimmune thyroid disease patients.
Purpose of the Study:
- To review and discuss the existing evidence for CXCL8's role in thyroid diseases.
- To evaluate CXCL8's potential as a prognostic marker in thyroid cancer.
- To consolidate findings on CXCL8's function in thyroid homeostasis and malignancy.
Main Methods:
- Review of experimental and clinical studies on CXCL8 in thyroid conditions.
- Analysis of data on CXCL8's function as a tumor promoter in various cancers.
- Synthesis of evidence regarding CXCL8's potential as a marker for thyroid cancer aggressiveness.
Main Results:
- CXCL8 is linked to thyroid homeostasis, but its role in thyroid diseases is not well-defined.
- Evidence suggests CXCL8 acts as a tumor promoter in several human cancers, with early promising findings in thyroid cancer.
- CXCL8 may serve as a marker of aggressiveness in thyroid cancer, similar to other malignancies.
Conclusions:
- CXCL8's function in thyroid homeostasis is supported by experimental data.
- CXCL8 shows potential as a tumor-promoting agent and marker of aggressiveness in thyroid cancer.
- Further research is needed to clarify CXCL8's role in various thyroid diseases.
Related Concept Videos
01:20Synthesis 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...
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...
01:27Hyperthyroidism 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...
01:23Hypothyroidism II: Pathophysiology
Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
01:28Graves' Disease I: Introduction
Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
01:24Graves 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...
01:23The 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...
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...