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Related Concept Videos

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
T Cell Types and Functions01:24

T Cell Types and Functions

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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

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Related Experiment Video

Updated: Jun 28, 2026

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
05:03

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica

Published on: October 28, 2022

Silica, apoptosis, and autoimmunity.

Jared M Brown1, Jean C Pfau, Mark A Pershouse

  • 1Department of Biomedical and Pharmaceutical Sciences, Center for Environmental Health Sciences, University of Montana, Missoula, Montana, USA.

Journal of Immunotoxicology
|October 30, 2008
PubMed
Summary

Occupational silica exposure is linked to autoimmune diseases like scleroderma and rheumatoid arthritis. This review explores mechanisms connecting silica exposure to the development and progression of these systemic autoimmune conditions.

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A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust
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A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust

Published on: January 6, 2023

Related Experiment Videos

Last Updated: Jun 28, 2026

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
05:03

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica

Published on: October 28, 2022

A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust
10:45

A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust

Published on: January 6, 2023

Area of Science:

  • Environmental Health
  • Immunology
  • Toxicology

Background:

  • Environmental exposures are implicated in autoimmune disease development.
  • Crystalline silica is one such environmental agent linked to systemic autoimmune diseases.
  • Epidemiological evidence suggests occupational silica exposure correlates with scleroderma, rheumatoid arthritis, and lupus.

Purpose of the Study:

  • To review human epidemiology data on silica exposure and systemic autoimmune disease.
  • To focus on potential mechanisms linking silica exposure to autoimmunity initiation and progression.

Main Methods:

  • Literature review of epidemiological studies.
  • Analysis of mechanistic pathways connecting silica exposure to autoimmune responses.

Main Results:

  • Growing epidemiological evidence supports a link between occupational silica exposure and various autoimmune diseases.
  • Few mechanistic studies currently exist to explain this association.
  • This review synthesizes existing data and proposes potential mechanisms.

Conclusions:

  • Silica exposure is a significant environmental factor associated with systemic autoimmune diseases.
  • Further mechanistic research is crucial to understand how silica triggers and advances autoimmunity.
  • Understanding these mechanisms may inform prevention and treatment strategies.