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Decay-accelerating factor regulates complement-mediated damage in the human atherosclerotic wall.

F Niculescu¹, H G Rus, R Vlaicu

¹Medical Clinic No. 1, Cluj-Napoca, Roumania.

Immunology Letters

|October 1, 1990

Summary

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Decay-accelerating factor (DAF) protects arterial walls from complement damage. However, DAF is insufficient to prevent complement activation in human atherosclerotic arteries.

Area of Science:

Immunology
Vascular Biology
Biochemistry

Background:

Decay-accelerating factor (DAF) is a membrane protein that inhibits complement pathways.
The role of DAF in the human atherosclerotic arterial wall is not fully understood.

Purpose of the Study:

To investigate the localization and function of DAF in human atherosclerotic arteries.
To determine if DAF protects against complement-mediated damage in the arterial wall.

Main Methods:

Immunohistochemistry and immunogold labeling to localize DAF in arterial tissue.
Western blotting to analyze DAF molecular weight.
Enzyme digestion and cell-based assays to assess DAF's protective role against complement-mediated lysis.

Main Results:

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DAF was found in the cells and connective tissue matrix of the arterial wall, with higher concentrations in fibrous plaques and intimal thickenings.
DAF co-localized with C5b-9 complement complexes on arterial cells and debris.
Blocking DAF significantly increased complement-mediated cell lysis from 10-15% to 60-70%.

Conclusions:

DAF plays a protective role against autologous complement activation in the arterial wall.
DAF's protective effect is insufficient to completely prevent complement activation in human atherosclerosis.