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Antiphospholipid syndrome infectious origin.

M Blank1, R A Asherson, R Cervera

  • 1Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.

Journal of Clinical Immunology
|March 5, 2004
PubMed
Summary
This summary is machine-generated.

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Infectious agents may trigger antiphospholipid syndrome (APS) by causing autoantibodies against beta 2-glycoprotein-I (beta 2GPI) through molecular mimicry, activating normally harmless immune responses.

Area of Science:

  • Immunology
  • Autoimmune Diseases
  • Microbiology

Background:

  • Antiphospholipid syndrome (APS) is defined by pathogenic autoantibodies targeting beta 2-glycoprotein-I (beta 2GPI).
  • The triggers for anti-beta 2GPI autoantibody production are unknown, but infections are suspected.
  • Individuals possess potentially autoreactive lymphocytes and natural antiphospholipid antibodies, which are usually inactive.

Purpose of the Study:

  • To explore the link between infections and antiphospholipid antibodies.
  • To discuss molecular mimicry as a potential mechanism in APS development.
  • To highlight the role of databases in understanding APS pathogenesis.

Main Methods:

  • Review of existing literature on APS, infectious agents, and molecular mimicry.

Related Experiment Videos

  • Analysis of experimental APS models demonstrating molecular mimicry.
  • Discussion of immunological principles related to autoimmunity and infection.

    • Main Results:

    • Experimental models show molecular mimicry between beta 2GPI and microbial structures can induce experimental APS.
    • Infections are associated with the presence of antiphospholipid antibodies.
    • Activation of normally quiescent autoreactive lymphocytes is a key consideration.

    Conclusions:

    • Molecular mimicry offers a plausible explanation for how microbial infections might initiate antiphospholipid syndrome.
    • Further research is needed to fully elucidate the role of infections in APS pathogenesis.
    • Databases can contribute valuable insights into the complex interactions driving APS.