Context
How do endothelial cells (ECs) protect themselves against damage by complement, particularly when they are present at the interface between blood and inflamed tissue? Cell surface proteins have evolved which prevent EC damage by the cytotoxic defence system, decay-accelerating factor (DAF), protectin (CD59) and membrane cofactor protein (MCP). DAF prevents the formation and accelerates the decay of complement 3 (C3) convertases, MCP binds to C3b and C4b promoting their degradation and CD59 inhibits the membrane-attack complex (MAC). How expression of these factors is controlled is not clear. The Hammersmith group has investigated control mechanisms since they are pertinent to the understanding of chronic inflammatory conditions such as rheumatoid arthritis and systemic lupus erythematosus. To test the hypothesis that inflammatory cytokines and complement(C) MACs play a role in the expression of DAF, CD59 and MCP, and to investigate the intracellular signalling pathway involved in DAF expression.