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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.
Concept and Mechanism of Autoimmune Diseases
The immune...
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Chronic Bowel Disorders: Introduction01:17

Chronic Bowel Disorders: Introduction

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Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
Irritable Bowel Syndrome (IBS) is a common disorder affecting the gastrointestinal tract. The distinctive feature is recurrent abdominal pain associated with altered bowel movements, manifesting as constipation, diarrhea, or fluctuating between both. The...
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Overview
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Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

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Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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T Cell Types and Functions01:24

T Cell Types and Functions

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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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Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
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Systemic autoinflammatory diseases.

Julie Krainer1, Sandra Siebenhandl1, Andreas Weinhäusel1

  • 1AIT Austrian Institute of Technology GmbH, Center for Health and Bioresources, Molecular Diagnostics, Giefinggasse 4, 1210, Vienna, Austria.

Journal of Autoimmunity
|February 6, 2020
PubMed
Summary
This summary is machine-generated.

Systemic autoinflammatory diseases (SAIDs) involve innate immune dysregulation. Identifying new diagnostic and treatment targets is crucial due to diagnostic delays and a significant percentage of undefined cases.

Keywords:
InflammasomesInflammationInnate immunityPeriodic feverSystemic autoinflammatory disease

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • Systemic autoinflammatory diseases (SAIDs) result from innate immune system dysregulation, causing recurrent inflammation.
  • Familial Mediterranean Fever, linked to the MEFV gene, is the most common SAID, with over 30 disease-associated genes identified since 1997.
  • A significant portion of patients (40-60%) present with phenotypes suggestive of SAIDs but lack a definitive diagnosis, termed undefined SAIDs (uSAIDs).

Purpose of the Study:

  • To provide a comprehensive overview of the pathogenesis and etiology of SAIDs.
  • To summarize current diagnostic and treatment strategies for SAIDs.
  • To highlight the complexity and the need for novel approaches in understanding and managing SAIDs.

Main Methods:

  • Review of existing literature on SAID pathogenesis, genetics, and clinical presentation.
  • Analysis of diagnostic criteria and current treatment modalities.
  • Discussion of emerging concepts, including polygenic origins and environmental influences.

Main Results:

  • SAIDs have a strong genetic basis, often involving single-gene mutations, but polygenic and multifactorial origins are increasingly recognized.
  • Diagnostic timelines can be lengthy (up to 7.3 years), emphasizing the need for improved diagnostic tools.
  • Environmental factors play a role in modulating SAID phenotypes.

Conclusions:

  • SAIDs represent a complex group of disorders requiring advanced methods to understand molecular mechanisms.
  • Elucidating the interplay between innate and adaptive immunity, and autoimmune and autoinflammatory pathways, is key.
  • Further research into novel diagnostic and therapeutic targets is imperative for improving patient outcomes.