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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.
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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.
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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...
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Graves Disease II: Pathophysiology01:24

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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,...
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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...
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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How do T cells mediate autoimmune thyroiditis?

Y C Kong1, M Bagnasco1, G W Canonica1

  • 1Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit MI 48201 USA; Istituto Scientifico di Medicina Intema, University of Genoa, 16132 Genoa, Italy.

Immunology Today
|October 8, 2014
PubMed
Summary
This summary is machine-generated.

T cells play a key role in experimental autoimmune thyroiditis (EAT) and Hashimoto's thyroiditis (HT). Research shows autoreactive T cells recognize thyroglobulin (Tg), driving thyroid destruction in susceptible individuals.

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Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Susceptibility to experimental autoimmune thyroiditis (EAT) is genetically determined by the mouse H-2 complex.
  • Thyroglobulin (Tg) is the primary autoantigen involved in initiating EAT.
  • T cells from susceptible mice are autoreactive, recognizing and proliferating in response to Tg.

Purpose of the Study:

  • To review evidence supporting the role of T cells in mediating autoimmune thyroiditis.
  • To explore the mechanisms by which T cells contribute to thyroid destruction.
  • To correlate findings from mouse models of EAT with human Hashimoto's thyroiditis (HT).

Main Methods:

  • Review of in vivo and in vitro studies on T-cell autoreactivity to mouse Tg.
  • Analysis of T-cell proliferation assays in response to human Tg in HT patients.
  • Examination of the capacity of murine T cells to differentiate and induce thyroiditis.

Main Results:

  • Confirmatory data from multiple laboratories demonstrate T-cell autoreactivity to mouse Tg, correlating with EAT susceptibility.
  • T cells from HT patients show in vitro proliferation in response to human Tg.
  • Murine T cells can expand, differentiate, and act as effector cells causing thyroiditis.

Conclusions:

  • T cells are confirmed mediators of autoimmune thyroiditis.
  • At least two distinct antigen-activated T-cell subsets appear to be involved in thyroid destruction.
  • Findings from mouse models and human HT patients highlight the pathogenic role of T cells.