Parham Chapter 2 Flashcards
Extracellular infections
pathogens that live and replicate in the spaces between human cells
Intracellular infections
pathogens that replicate inside human cells
Complement System (Complement)
set of plasma proteins that act in a cascade of reactions to attack extracellular forms of pathogens. Many of them are serine proteases. As a result of complement activation, pathogens become coated with complement components, which can either kill the pathogen directly or facilitate its engulfment and destruction by phagocytes.
Complement activation
the initiation of pathogens of a series of reactions involving the complement components of plasma, leading to the death and elimination of the pathogen
Complement component 3 (C3)
the central and most important component of the complement system. Also called C3 for short
Protease
Any of various enzymes, including the proteinases and peptidases, that catalyze the hydrolytic breakdown of proteins.
an enzyme that is a catalyst in the breakdown of peptide bonds that join the amino acids in a protein.
proteolysis
a process in which water added to the peptide bonds of proteins breaks down the protein molecule into simpler substances. Numerous enzymes may catalyze this process. The action of mineral acids and heat also may induce proteolysis.
Complement fixation
the covalent attachment of C3B or C4B to pathogen surfaces, which is a central feature of the action of complement because it facilitates phagocytosis of the pathogen.
Alternate pathway of complement activation
one of the three pathways of complement activation. It is triggered by the presence of infection but does not involve antibody.
Lectin pathway of complement activation
one of the three pathways of complement activation. It is activated by the binding of a mannose-binding lectin present in blood plasma to mannose containing peptidoglycans on bacterial surfaces
Classical pathway of complement activation
one of the three pathways of complement activation. It is activated by antibody bound to antigen, and involves complement components C1, C4, and C2 in the generation of the classical C3 and C5 convertases.
iC3 or C3(H2O)
the product formed when the thioester bond of complement component C3 is hydrolyzed by water; form of the complement protein C3 produced in the first step in the alternative pathway of complement activation in which a thioester bond is hydrolyzed but the molecule is not cleaved
factor B
plasma protein that binds to C3(H2O) or C3b and is cleaved to form part of the C3 convertases (C3(H2O)Bb and C3bBb) in the alternative pathway of complement activation.
factor D
plasma protease that cleaves factor B to Bb and Ba in the alternative pathway of complement activation.
C3 convertases
proteolytic enzymes that are formed during complement activation and cleave complement component C3 to C3b and C3a, thereby enabling C3b to bond covalently to antigens.
Alternate C3 convertase
the C3 convertase of the alternative pathway of complement activation. It is composed of C3 of C3 (H2O) bound to proteolytically active Bb (C3Bb or C3(H2O)Bb) and cleaves C3 into C3a and C3b.
Complement control proteins
any of a diverse group of proteins that inhibit complement activation at various stages and by different mechanisms
Properdin (factor P)-
the complement factor that stabilizes the alternative C3 convertase; blood protein that helps to activate the alternative pathway of complement activation. It binds to and stabilizes the alternative pathway C3 and C5 convertases on the surface of bacterial cells.
Factor H
complement regulatory protein of plasma that inactivates the C3 converatse of the alternative pathway and C5 convertases by binding to C3b and rendering it susceptible to cleavage by factor I to produce inactive iC3b.
Factor I
protease that regulates complement action by cleaving C3b and C4b into inactive forms
Decay-accelerating factor (DAF)
cell surface protein that prevents complement activation on human cells. DAF binds to C3 converatses of both the alternative and classical pathways of complement activation and, by displacing Bb and C2a, respectively, prevents their action
Membrane co-factor protein (MCP)
complement regulatory protein on human cells that promotes the inactivation of C3b and C4b by factor I.