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Updated: Aug 8, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
CD59 (homologous restriction factor 20), a plasma membrane protein that protects against complement C5b-9 attack, in
P S Seifert1, I Roth, W Schmiedt
1Institute for Medical Microbiology, Johannes Gutenberg University, Mainz, FRG.
Insights
CD59, a protein that prevents complement C5b-9 insertion, is present on cells in human atherosclerotic lesions. Its expression varies, suggesting complement attack primarily targets smooth muscle cells.
Area of Science:
- Immunology
- Pathology
- Cardiovascular Research
Background:
- Blood cells express CD59 (homologous restriction factor 20), inhibiting complement C5b-9 membrane insertion.
- Membranous C5b-9 has been detected in human atherosclerotic lesions.
- The cellular distribution of CD59 in these lesions was previously unknown.
Purpose of the Study:
- To investigate the presence and cellular localization of CD59 in human atherosclerotic lesions using immunohistochemistry.
- To determine if CD59 expression correlates with complement deposition in lesions.
Main Methods:
- Immunohistochemistry was performed on human atherosclerotic lesion specimens.
- A monoclonal anti-CD59 antibody was used for staining.
- Co-localization studies were conducted with markers for macrophages (CD14), T lymphocytes (CD7), endothelial cells (factor VIII related antigen), and smooth muscle cells (alpha actin, muscle myosin).
Main Results:
- CD59 staining was observed in nearly all lesion specimens, co-localizing with macrophages, T lymphocytes, endothelial cells, and smooth muscle cells.
- Endothelial cells showed more intense CD59 staining than other cell types.
- CD59 expression was variable, with some smooth muscle cells negative and some areas exhibiting C5b-9 deposits despite CD59 presence.
Conclusions:
- CD59 (HRF20) is constitutively expressed on endothelium and its expression is regulated in smooth muscle cells within atherosclerotic lesions.
- The findings suggest that complement C5b-9 attack in atherosclerotic lesions is most likely to occur on smooth muscle cells.
- CD59 distribution indicates a complex interplay between complement regulation and cellular components in atherogenesis.
Abstract:
Blood cells express a cell membrane protein, termed homologous restriction factor 20 (HRF20) and identical to CD59, that can inhibit complement C5b-9 insertion into their membranes. In this report, we investigated by immunohistochemistry whether CD59 was present on cells in human atherosclerotic lesions since membranous C5b-9(m) has been found in lesions. Using a monoclonal anti-CD59 antibody, a cellular CD59 staining pattern was apparent in nearly all lesion specimens. CD59 stain co-localised with macrophage (CD14), T lymphocyte (CD7), endothelial cell (anti-factor VIII related antigen) and smooth muscle cell cytoskeletal-specific antigens (anti-alpha actin and muscle myosin). Endothelial cells always exhibited a more intense stain than the other cell types. CD59 antigen was not localised to any one area of the lesions. Usually CD59-positive cells occurred in clusters rather than as randomly spaced individual cells. CD59 did not stain all cells of the lesion and in particular did not appear to stain all smooth muscle cells. Areas of CD59-negative cells were sometimes observed to exhibit a cellular C5b-9 staining pattern. C5b-9 deposits were also observed in CD59-positive regions. Normal saphenous vein stained strongly for CD59 at the endothelial lining and weakly in the media. Capillaries in atherosclerotic intima always stained strongly for CD59. We conclude that HRF20 is constitutively expressed on endothelium and is under regulatory control in smooth muscle cells. Cellular C5b-9 attack in atherosclerotic lesions is therefore most likely to occur on smooth muscle cells.
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