Complement C3-C5 Convertases

About: Complement C3-C5 Convertases is a research topic. Over the lifetime, 97 publications have been published within this topic receiving 13061 citations.

Complement: a key system for immune surveillance and homeostasis

Abstract: Nearly a century after the significance of the human complement system was recognized, we have come to realize that its functions extend far beyond the elimination of microbes. Complement acts as a rapid and efficient immune surveillance system that has distinct effects on healthy and altered host cells and foreign intruders. By eliminating cellular debris and infectious microbes, orchestrating immune responses and sending 'danger' signals, complement contributes substantially to homeostasis, but it can also take action against healthy cells if not properly controlled. This review describes our updated view of the function, structure and dynamics of the complement network, highlights its interconnection with immunity at large and with other endogenous pathways, and illustrates its multiple roles in homeostasis and disease.

Complement evasion by human pathogens

Abstract: The human immune system has developed an elaborate network of cascades for dealing with microbial intruders. Owing to its ability to rapidly recognize and eliminate microorganisms, the complement system is an essential and efficient component of this machinery. However, many pathogenic organisms have found ways to escape the attack of complement through a range of different mechanisms. Recent discoveries in this field have provided important insights into these processes on a molecular level. These vital developments could augment our knowledge of the pathology and treatment of infectious and inflammatory diseases.

The membrane attack complex of complement.

Abstract: Cell-killing mechanisms are essential components of host defense against infectious agents, parasites, and malignant cells. We distinguish humoral and cellular killing mechanisms. Complement utilizes specific proteins to assemble its killer molecule. Macrophages generate active oxygen radicals that injure target membranes. Lymphocytes, like complement, use protein molecules as tools in the cellular cytotoxicity reaction. As will be suggested at the conclusion of this chapter, considerable similarity between the structure of the cytolytic apparatus of complement and that of lymphocytes has recently come to light. An in-depth knowledge of the structure and function of the killer molecule of complement may therefore facilitate elucidation of the cell-killing mechanism of lymphocytes. Complement encompasses 20 proteins, not including the various cell­ surface complement receptors and regulatory proteins. Only 5 of these 20 proteins participate directly in cell killing-C5, C6, C7, C8, and C9-and none has enzymatic activity, proteolytic or lipolytic. Upon activation of C5, the 5 proteins interact in a sequential manner and fuse into a macromo­ lecular organization, called the membrarie attack complex or MAC. Fusion brings forth hydrophobic sites through which the complex inserts itself into the hydrocarbon core of lipid membranes. There it forms transmembrane channels, the largest of which constitutes tubular poly C9. Activation of C5 is accomplished by a highly specific serine protease, C5 convertase, itself an assembly of three protein molecules. Thus, formation of the MAC is initiated enzymatically, but this enzyme does not participate in actual membrane attack, which is entirely a physicochemical process.