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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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Graves' Disease I: Introduction01:28

Graves' 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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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...
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 25, 2026

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

TLR-4 expression and decrease in chronic inflammation: indicators of aggressive follicular thyroid carcinoma.

Jaana Hagström1, Annukka Heikkilä, Päivi Siironen

  • 1Department of Pathology, Haartman Institute, University of Helsinki and HUSLAB, Helsinki, Finland. jaana.hagstrom@hus.fi

Journal of Clinical Pathology
|January 24, 2012
PubMed
Summary

Toll-like receptor 4 (TLR-4) expression and inflammation levels in follicular thyroid cancer can indicate aggressive disease. Varying TLR-4 levels and a lack of inflammation are associated with metastatic potential.

Related Experiment Videos

Last Updated: May 25, 2026

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Area of Science:

  • Endocrinology
  • Immunology
  • Oncology

Background:

  • Follicular thyroid carcinoma typically has a good prognosis with rare metastases.
  • Toll-like receptors (TLRs) play complex roles in immunity and cancer, with controversial effects on tumourigenesis.
  • Chronic inflammation is implicated in the development of various cancers.

Purpose of the Study:

  • To investigate the clinical significance of Toll-like receptor 2 (TLR-2), Toll-like receptor 4 (TLR-4), and CD45 in follicular thyroid neoplasias.
  • To correlate these markers with tumour aggressiveness and metastatic potential.

Main Methods:

  • Immunohistochemical analysis of TLR-2 and TLR-4 expression in 127 follicular thyroid neoplasms (adenomas and carcinomas).
  • Quantification of CD45-positive lymphocytes to assess chronic inflammation within and around tumours.
  • Correlation of marker expression and inflammation with clinical variables, including metastasis.

Main Results:

  • Both high and low TLR-4 expression in carcinomas were linked to metastatic and aggressive disease.
  • TLR-4 expression was significantly higher in oxyphilic adenomas and carcinomas.
  • Reduced chronic inflammation outside the primary tumour correlated with metastasized carcinomas.

Conclusions:

  • Aberrant TLR-4 expression and diminished inflammation are indicators of aggressive follicular thyroid cancer.
  • These findings suggest potential biomarkers for predicting disease behavior in follicular thyroid neoplasias.