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Related Concept Videos

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...
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...
Antibody Structure01:10

Antibody Structure

Overview
Antibodies, also known as immunoglobulins (Ig), are essential players of the adaptive immune system. These antigen-binding proteins are produced by B cells and make up 20 percent of the total blood plasma by weight. In mammals, antibodies fall into five different classes, which each elicits a different biological response upon antigen binding.
The Y-Shaped Structure of Antibodies Consists of Four Polypeptide Chains
Antibodies consist of four polypeptide chains: two identical heavy...
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...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Autoantibody heritability in thyroiditis: IgG subclass contributions.

Ingrid M Outschoorn1, Monica V Talor, William H Hoffman

  • 1Instituto de Salud Carlos III, Centro Nacional de Microbiologia, Unidad de Respuesta Inmune, Majadahonda, Madrid, Spain. ioutscho@isciii.es

Autoimmunity
|October 2, 2010
PubMed
Summary
This summary is machine-generated.

Regression of offspring on mid-parent (ROMP) analysis revealed significant familial links in autoimmune thyroid disease, particularly thyrotoxicosis. This method may help predict disease onset by examining IgG subclasses and autoantibodies.

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Published on: December 15, 2011

Area of Science:

  • Immunogenetics
  • Autoimmune Diseases
  • Pediatric Endocrinology

Background:

  • Autoimmune thyroid diseases (ATD) like thyrotoxicosis (TT) and chronic lymphocytic thyroiditis (CLT) have a complex etiology involving genetic and environmental factors.
  • The role of specific immunoglobulin G (IgG) subclasses in the heritability of ATD requires further elucidation.
  • Understanding familial aggregation patterns can inform disease prediction and prevention strategies.

Purpose of the Study:

  • To investigate the role of IgG subclasses in the familial transmission of autoimmune thyroid disease using the regression of offspring on mid-parent (ROMP) technique.
  • To quantitatively assess autoantibodies to thyroglobulin (Tg) across IgG subclasses in affected individuals and their parents.
  • To identify potential predictors of disease onset and progression based on immunoglobulin profiles.

Main Methods:

  • Employed the regression of offspring on mid-parent (ROMP) screening technique.
  • Quantitatively assayed total-restricted and subclass-restricted autoantibodies to thyroglobulin (Tg) for IgG subclasses.
  • Analyzed data from affected siblings and their parents for children and adolescents with ATD.

Main Results:

  • A significant correlation between proband anti-Tg titers and parental titers was observed in thyrotoxicosis (TT) (R(2) = 0.569, p = 0.001), but not in chronic lymphocytic thyroiditis (CLT).
  • A particularly strong correlation was found in TT patients of African-American ancestry (R(2) = 0.9863, p = 0.0007).
  • Individual IgG subclass contributions to total IgG titers were examined, revealing potential independent influences.

Conclusions:

  • ROMP is a rapid and effective method for assessing familial aggregation of autoantibodies in ATD, even with small patient cohorts.
  • IgG subclass analysis via ROMP can identify quantifiable parameters useful for predicting ATD onset and progression.
  • The findings highlight the significant genetic component in thyrotoxicosis, especially within specific ancestral groups.