Decay-accelerating factor protects human tumor cells from complement-mediated cytotoxicity in vitro.

Statin-induced expression of decay-accelerating factor protects vascular endothelium against complement-mediated injury.

Complement-mediated vascular injury is important in the pathophysiology of atherosclerosis and myocardial infarction. Because recent evidence shows that statins have beneficial effects on endothelial cell (EC) function independent of lipid lowering, we explored the hypothesis that statins modulate vascular EC resistance to complement through the upregulation of complement-inhibitory proteins. H...

Complement Attack Protecting Cells from Autologous Factor and Membrane Cofactor Protein in Cooperation Between Decay-Accelerating

Coexistence of autologous antibodies and decay-accelerating factor, an inhibitor of complement, on human renal tumor cells.

Autologous immunoglobulin was detected on the cell surface of tumor cells freshly isolated from cancerous kidneys of patients with renal cell carcinoma by flow cytometry after staining with murine anti-human IgG monoclonal antibodies. Cells isolated in parallel from macroscopically normal regions of the tumorous kidneys were not specifically stained with the anti-human IgG reagents. In further ...

Induction of decay-accelerating factor by thrombin through a protease-activated receptor 1 and protein kinase C-dependent pathway protects vascular endothelial cells from complement-mediated injury.

There is increasing evidence for functional crosstalk between inflammatory and thrombotic pathways in inflammatory vascular diseases such as atherosclerosis and vasculitis. Thus, complement activation on the endothelial cell (EC) surface during inflammation may generate thrombin via the synthesis of tissue factor. We explored the hypothesis that thrombin induces EC expression of the complement-...

Induction of decay-accelerating factor by cytokines or the membrane-attack complex protects vascular endothelial cells against complement deposition.

Vascular endothelium is continuously exposed to complement-mediated challenge, and this is enhanced during inflammation. Although the complement-regulatory proteins decay-accelerating factor (DAF), CD59, and membrane cofactor protein (MCP) protect endothelial cells (ECs) against complement-mediated injury, the control of their expression and relative contributions to vascular protection is uncl...