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Published on: January 13, 2012
Anti-heat shock protein 60 autoantibodies induce atherosclerosis in apolipoprotein E-deficient mice via endothelial
Georgios Foteinos1, Ali R Afzal, Kaushik Mandal
1Department of Cardiac and Vascular Sciences, St. George's University of London, Cranmer Terrance, London SW17 0RE, UK.
Circulation
|August 24, 2005
Summary
Autoantibodies against heat shock protein 60 (HSP60) can cause atherosclerosis. Blocking these autoantibodies with F(ab)2 segments prevents lesion development in mice, suggesting a causal role for HSP60 autoimmunity in atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Research
- Atherosclerosis Pathogenesis
Background:
- A positive association exists between anti-heat shock protein 60 (HSP60) autoantibodies and human atherosclerosis.
- The causal role of these autoantibodies in atherosclerosis development remains unclear.
Purpose of the Study:
- To investigate the causal role of anti-HSP60 autoantibodies in atherosclerosis development.
- To determine the specific mechanisms by which anti-HSP60 autoantibodies induce atherosclerotic lesions.
Main Methods:
- Isolated anti-HSP60 autoantibodies from coronary heart disease patients.
- Injected autoantibodies and a specific monoclonal antibody (II-13) into apolipoprotein E-deficient mice.
- Administered F(ab)2 segments to block antibody effects.
Main Results:
- Injection of anti-HSP60 autoantibodies significantly increased atherosclerotic lesions in mice.
- Monoclonal antibody II-13, targeting HSP60 residues 288-366, induced lesions, endothelial damage, and immune cell accumulation.
- F(ab)2 segments derived from the antibody blocked II-13-induced atherosclerosis.
Conclusions:
- Autoantibodies targeting HSP60 residues 288-366 induce atherosclerosis through autoimmune reactions against arterial endothelial cells.
- F(ab)2 segments derived from these autoantibodies can prevent the development of atherosclerosis.
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