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Monogenic polyautoimmunity in primary immunodeficiency diseases.

Gholamreza Azizi1, Reza Yazdani2, Wiliam Rae3

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Autoimmunity Reviews
|August 15, 2018
PubMed
Summary

Genetic primary immunodeficiency diseases (PIDs) impair immune tolerance, increasing risks of multiple autoimmune diseases (polyautoimmunity). This review details autoimmunity mechanisms and polyautoimmunity in specific PIDs.

Keywords:
AutoimmunityCTLA4IPEXLRBAPolyautoimmunityPolyglandular autoimmune syndromesPrimary immunodeficiencyRegulatory T cell

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Area of Science:

  • Immunology
  • Genetics
  • Autoimmunity

Background:

  • Primary immunodeficiency diseases (PIDs) are genetic disorders affecting the immune system.
  • PIDs increase susceptibility to infections and non-infectious complications like autoimmunity.
  • Monogenic PIDs with impaired immune tolerance regulation are at high risk for polyautoimmunity.

Purpose of the Study:

  • To review the mechanisms of autoimmunity in primary immunodeficiency diseases.
  • To characterize polyautoimmunity in specific monogenic PIDs.

Main Methods:

  • Literature review of monogenic PIDs associated with autoimmunity.
  • Analysis of genetic defects impacting immune tolerance.
  • Characterization of polyautoimmunity in selected PIDs.

Main Results:

  • Specific monogenic PIDs result from mutations in genes crucial for immune tolerance.
  • These PIDs exhibit a high propensity for developing polyautoimmunity.
  • Examples include IPEX, LRBA deficiency, CTLA4 deficiency, APECED, ALPS, and PKCδ deficiency.

Conclusions:

  • Understanding autoimmunity mechanisms in PIDs is crucial for diagnosis and management.
  • Identifying genetic defects aids in predicting and addressing polyautoimmunity risk.
  • Further research into these PIDs can reveal novel therapeutic targets.