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Apoptotic cells with oxidation-specific epitopes are immunogenic and proinflammatory
Mi-Kyung Chang1, Christoph J Binder, Yury I Miller
1Division of Endocrinology, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093, USA. m7chang@ucsd.edu
The Journal of Experimental Medicine
|December 8, 2004
Summary
Apoptotic cells release oxidized phospholipids (OxPLs), triggering autoimmune responses and inflammation. These findings reveal a link between cell death, oxidation, and atherosclerosis development.
Area of Science:
- Cardiovascular Science
- Immunology
- Cell Biology
Background:
- Oxidation of low-density lipoprotein (LDL) contributes to atherosclerosis.
- Apoptotic cells display oxidized moieties on their surface membranes.
Purpose of the Study:
- To investigate the role of oxidized phospholipids (OxPLs) generated during apoptosis in immune responses and inflammation.
- To determine if OxPLs from apoptotic cells can induce autoimmune responses and activate endothelial cells.
Main Methods:
- Mass spectrometry to quantify OxPLs in apoptotic vs. viable cells.
- Immunization of mice with apoptotic cells to assess autoantibody production.
- Cytokine release assays from splenocyte cultures.
- Endothelial cell activation assays measuring monocyte adhesion.
Main Results:
- Apoptotic cell membranes showed increased levels of biologically active OxPLs compared to viable cells.
- Immunization with apoptotic cells induced high autoantibody titers to oxidation-specific epitopes, including OxPLs.
- Splenocytes from immunized mice released significant levels of Th1 and Th2 cytokines.
- OxPLs from apoptotic cells activated endothelial cells, promoting monocyte adhesion.
Conclusions:
- Apoptotic cell death generates immunogenic OxPLs, potentially initiating autoimmune responses.
- OxPLs from apoptotic cells contribute to local inflammation by activating endothelial cells and promoting monocyte recruitment.
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