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Apoptosis and the antiphospholipid syndrome
J Rauch1, R Subang, P D'Agnillo
1Division of Rheumatology, Department of Medicine, The Montreal General Hospital Research Institute, McGill University, Montreal, Quebec, H3G 1A4, Canada. mdrh@musica.mcgill.ca
Journal of Autoimmunity
|September 2, 2000
Summary
Apoptotic cells, not viable cells, may be the natural target for antiphospholipid autoantibodies (APA). These antibodies may be induced by beta 2-glycoprotein I binding to apoptotic cells, potentially playing a role in autoimmune diseases.
Area of Science:
- Immunology
- Autoimmunity
- Cell Biology
Background:
- Antiphospholipid autoantibodies (APA) are implicated in autoimmune diseases like antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE).
- The precise in vivo target and immunogen for APA remain unclear, though a complex of anionic phospholipid (PL) and beta 2-glycoprotein I (beta 2-GPI) is implicated.
Purpose of the Study:
- To review evidence suggesting apoptotic cells serve as natural targets and potential immunogens for APA.
- To explore the role of beta 2-glycoprotein I (beta 2-GPI) binding to apoptotic cells in generating APA epitopes.
Main Methods:
- Review of existing literature on APA, beta 2-GPI, and apoptosis.
- Analysis of studies investigating the binding of beta 2-GPI to apoptotic cells.
- Discussion of potential epitope generation through cell oxidation.
Main Results:
- Anionic phospholipids redistribute to the outer cell membrane during apoptosis, becoming accessible targets.
- Beta 2-glycoprotein I selectively binds to apoptotic cells, creating epitopes recognized by APA.
- Non-intravenous routes of antigen exposure and oxidation may contribute to APA induction.
Conclusions:
- Apoptotic cells are strongly supported as targets for APA.
- Apoptotic cells may play a significant role in the induction of APA, contributing to autoimmune pathogenesis.