Decay-Accelerating Factor and Membrane Cofactor Protein

摘要: Cells exposed to plasma proteins are frequently under attack from the complement system. This can arise either as a bystander process classical or alternative pathways of activation initiated during immune response foreign particles and organisms constant tick-over pathway. Thus, it is critical for cell regulate pathway on its own surface. The proteins, H C4 binding protein (C4bp), in conjugation with serine protease I, function this end. Additionally, cells possess number membrane deposited their surfaces; largest group, focused C3 convertases, consists C3b/C4b receptor (CR1), decay-accelerating factor (DAF), cofactor (MCP). CR1, although has both activity serves I-mediated cleavage C3b C4b, acts mainly extrinsically C3b-bearing complexes. DAF exerts intrinsically itself (see below). Indeed, lack blood disease paroxysmal nocturnal hemoglobinuria (PNH) leads an increased sensitivity these cells. Purified MCP also convertases through I activity. same approximate size overall structure DAF, hence might control formed cell. chapter reviews detail structure, at DNA levels, two regulatory glycoproteins, MCP, discusses physiological roles protecting damage by autologous complement.