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Related Concept Videos

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...
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 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...
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...
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...
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...

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Related Experiment Video

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Human In Vitro Suppression as Screening Tool for the Recognition of an Early State of Immune Imbalance
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Published on: July 22, 2011

Decrease in proportion of CD19+ CD24(hi) CD27+ B cells and impairment of their suppressive function in Graves'

Bingbing Zha1, Luman Wang, Xiaoming Liu

  • 1Department of Endocrinology and Metabolism, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.

Plos One
|November 29, 2012
PubMed
Summary
This summary is machine-generated.

Interleukin-10-producing B cells (B10 cells), a CD24(hi)CD27(+) B cell subpopulation, are reduced in Graves' disease patients. Their impaired suppressive function may contribute to Graves' disease pathogenesis.

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Functional Characterization of Regulatory Macrophages That Inhibit Graft-reactive Immunity

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Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Interleukin-10-producing B cells (B10 cells) regulate immune responses and are implicated in autoimmune diseases.
  • The specific role of B10 cells in Graves' disease (GD) pathogenesis is currently unknown.

Purpose of the Study:

  • To investigate the role and function of B10 cells in Graves' disease.
  • To identify the B10 cell subpopulation in human peripheral blood.

Main Methods:

  • Characterization of B10 cells as CD19(+)CD24(hi)CD27(+) B cells.
  • Flow cytometry analysis of B10 cell proportions in new-onset GD, recovered GD, and healthy individuals.
  • Assessment of the suppressive function of B10 cells on CD4(+) T cell proliferation and cytokine production (TNF-α, IFN-γ) via IL-10-dependent and -independent pathways.

Main Results:

  • B10 cells were identified as CD19(+)CD24(hi)CD27(+) B cells.
  • Proportions of B10 cells were significantly lower in new-onset GD patients, restoring upon recovery.
  • Impaired suppressive function of B10 cells on CD4(+) T cell proliferation and cytokine production was observed in both new-onset and recovered GD patients compared to healthy controls.

Conclusions:

  • CD19(+)CD24(hi)CD27(+) B cells exhibit immunosuppressive capacity, partly via IL-10 production.
  • Impairment of B10 cell immunosuppressive function may contribute to the pathogenesis and relapse of Graves' disease.