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Related Concept Videos

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...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism 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...
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...
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...
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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Emerging mechanisms and targetable pathways in immune checkpoint inhibitor‑associated thyroid dysfunction: From

Tianying Zhang1, Hengtong Han2, Hao Shi1

  • 1The First School of Clinical Medicine, Lanzhou University, Lanzhou 730000, China.

Critical Reviews in Oncology/Hematology
|July 9, 2026
PubMed
Summary

Immune checkpoint inhibitors (ICIs) can cause thyroid dysfunction. This review proposes a new framework for predicting and managing ICI-related thyroid dysfunction to improve immunotherapy safety.

Keywords:
Epigenetic regulationGut-thyroid axisImmune checkpoint inhibitorsTargeted therapyThyroid dysfunction

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Area of Science:

  • Oncology
  • Immunology
  • Endocrinology

Background:

  • Immune checkpoint inhibitors (ICIs) enhance anti-cancer immunity but can lead to immune-related thyroid dysfunction (ICI-TD).
  • ICI-TD presents with diverse clinical manifestations, ranging from subclinical changes to thyroid storm, stemming from immune tolerance breakdown and autoreactive responses.
  • Different ICIs (e.g., anti-PD-1/PD-L1, anti-CTLA-4) exhibit distinct thyroid toxicity profiles, with combination therapies potentially increasing risks and accelerating onset.

Purpose of the Study:

  • To systematically review the mechanisms underlying ICI-TD.
  • To explore emerging targeted strategies for managing ICI-TD.
  • To propose a novel "mechanism-prediction-intervention" framework for optimizing ICI-TD management.

Main Methods:

  • Systematic review of emerging mechanisms including immune cell interactions, epigenetic regulation, and the gut-thyroid axis.
  • Review of targeted therapeutic strategies such as conditionally activated antibodies, Fc engineering, chemokine receptor targeting, and cytokine neutralization.
  • Conceptualization of a predictive and interdisciplinary management framework.

Main Results:

  • ICI-TD mechanisms involve complex immune cell crosstalk, epigenetic modifications, and the gut-thyroid axis.
  • Novel therapeutic strategies show promise for mitigating ICI-TD.
  • Current management is often reactive, relying on monitoring and hormone replacement, with delayed interventions.

Conclusions:

  • A "mechanism-prediction-intervention" framework integrating multi-omics data can enable early warning and hierarchical management of ICI-TD.
  • This approach is expected to optimize the risk-benefit ratio of immunotherapy.
  • Implementing this framework will enhance the safety and efficacy of cancer immunotherapy.