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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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Immunodeficiency Diseases01:25

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Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Related Experiment Video

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Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity
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Autoimmunity in primary T-cell immunodeficiencies.

Gholamreza Azizi1,2, Alireza Ghanavatinejad3, Hassan Abolhassani2,4

  • 1a Department of Laboratory Medicine , Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences , Karaj , Iran.

Expert Review of Clinical Immunology
|April 12, 2016
PubMed
Summary

Primary T-cell immunodeficiencies (PID) can lead to severe infections and non-infectious issues like autoimmunity. This review explores autoimmune disorders linked to various T-cell PIDs.

Keywords:
Primary immunodeficiencyT cellautoimmunityregulatory T celltolerance

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Area of Science:

  • Immunology
  • Genetics
  • Clinical Medicine

Background:

  • Primary immunodeficiency diseases (PID) encompass over 270 genetic disorders affecting the immune system.
  • T-cell PIDs typically manifest early in life, often presenting as combined T- and B-cell deficiencies.
  • Patients with T-cell PID face risks of life-threatening infections and non-infectious complications.

Purpose of the Study:

  • To review the proposed mechanisms of autoimmunity in primary T-cell immunodeficiencies.
  • To summarize the literature on autoimmune disorders associated with different types of T-cell PIDs.

Main Methods:

  • Literature review of scientific articles and case studies.
  • Analysis of proposed pathogenic mechanisms for autoimmunity in T-cell PIDs.
  • Categorization of autoimmune manifestations based on specific T-cell PID types.

Main Results:

  • Autoimmunity is a significant non-infectious complication of T-cell PIDs.
  • Immune thrombocytopenic purpura (ITP) and autoimmune hemolytic anemia (AIHA) are frequent autoimmune disorders observed.
  • Various T-cell PIDs are associated with distinct autoimmune conditions.

Conclusions:

  • Understanding the link between T-cell PIDs and autoimmunity is crucial for patient management.
  • Further research into the mechanisms of autoimmunity in PID is warranted.
  • Early identification and treatment of autoimmune complications can improve outcomes for patients with T-cell PIDs.