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Related Concept Videos

Autoimmune Disorders01:29

Autoimmune Disorders

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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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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
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Related Experiment Video

Updated: Sep 13, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
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Pathogenesis of Autoimmunity/Systemic Lupus Erythematosus (SLE).

Shunichi Shiozawa1,2,3

  • 1Institute for Rheumatic Diseases, 60-14 Okuikeminamicho, Ashiya 659-0004, Japan.

Cells
|July 25, 2025
PubMed
Summary

Systemic Lupus Erythematosus (SLE) is caused by DOCK8-positive T follicular helper (Tfh) cells, which are generated after repeated infections. These cells trigger autoimmunity and can be targeted for SLE treatment.

Keywords:
T follicular helper cells (Tfh cells)autoimmunitypathogenesissystemic lupus erythematosus (SLE)

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Area of Science:

  • Immunology
  • Rheumatology
  • Autoimmune Diseases

Background:

  • Systemic Lupus Erythematosus (SLE) is defined by diverse autoantibodies and organ damage.
  • Identifying the specific factor causing SLE requires it to induce, persist in, and resolve with SLE.
  • Previous candidates like interferon-alpha and BAFF (B cell activating factor) did not fully meet these criteria.

Purpose of the Study:

  • To review and identify the definitive causative factor of Systemic Lupus Erythematosus (SLE).
  • To evaluate candidate factors against established criteria for disease causation.
  • To explore the role of T follicular helper (Tfh) cells and infection in SLE pathogenesis.

Main Methods:

  • Review of existing literature on potential SLE-causing factors.
  • Analysis of genetic models (BXSB mice, sanroque mice) and their association with SLE.
  • Investigation of T follicular helper (Tfh) cell populations, including DOCK8-positive Tfh cells, in SLE pathogenesis.
  • Application of self-organized criticality theory to understand infection-driven autoimmunity.

Main Results:

  • Genetic factors like duplicated TLR7 and the Sle1 gene are implicated in SLE development.
  • Mutations affecting ICOS regulation lead to increased Tfh cells, IL-21, and SLE.
  • DOCK8-positive Tfh cells, generated post-infection (e.g., SARS-CoV-2), fulfill all criteria for causing SLE.
  • Therapies targeting DOCK8-positive Tfh cells or DOCK8 itself showed promise in reducing SLE manifestations.

Conclusions:

  • DOCK8-positive Tfh cells, arising from repeated infections, are identified as the causative factor for SLE.
  • These autoreactive Tfh cells drive autoantibody production and SLE pathogenesis.
  • Targeting DOCK8-positive Tfh cells represents a potential therapeutic strategy for SLE.