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.
Complement control protein (CCP) modules
family of structurally similar protein modules found in many of the proteins that regulate complement activity
Regulators of complement activation (RCA)
proteins that regulate the activity of complement and contain one or more copies of a particular structural motif of -60 amino acid residues called the CCP (complement control protein) motif. The CCP motif is also called a sushi domain because of its similarity in shape to a slice of a sushi roll.
Macrophage
large mononuclear phagocytic cell resident in most tissues. Macrophages are derived from blood monocytes and contribute to innate immunity and early non-adaptive phases of host defense. They function as professional antigen presenting cells and as effector cells in humoral and cell mediated immunity.
Kupffer cells
phagocytic cells of the liver that line the hepatic sinusoids.
Complement Receptors (CRs)
cell surface proteins on various cell types that recognize and bind complement proteins bound to antigens. Complement receptors on phagocytes facilitate the phagocytic engulfment of pathogens coated with complement. Complement receptors include CR1, CR2, CR3, CR4, and the receptor for C1q.
Complement receptor 1 (CR1)
a
Complement receptor 2 (CR2)
a
Complement receptor 3 (CR3)
a
Complement receptor 4 (CR4)
a
Opsonization
the coating of the surface of a pathogen or other particle with any molecule that makes it more readily ingested by phagocytes. Antibody and complement opsonize extracellular bacteria for phagocytosis by neutrophils and macrophages because the phagocytic cells carry receptors for these molecules.
Alternative C5 convertase
the C5 convertase of the alternate pathway of complement activation. It is composed of two molecules of C3b bound to Bb (C3b2Bb) and cleaves C5 into C5a and C5b.
Membrane-attack complex
the complex of terminal complement components that forms a pore in the membrane of the target cell, damaging the membrane and leading to cell lysis.
CD59 (protectin)
complement control protein; protein on the surface of human cells that prevents the assembly of the complement membrane-attack complex on the cell surface, thus protecting human cells against complement mediated lysis.
Paroxysmal nocturnal hemoglobinuria (PNH)
a disease in which the complement regulatory proteins CD59 and DAF are defective, so that complement activation leads to episodes of spontaneous hemolysis. The defect is in the attachment of CD59 and DAF to cell membranes via a glycolipid anchor.
Anaphylatoxins
complement fragments C3a and C5a, which are produced during complement activation. They act to induce inflammation, recruiting fluid and inflammatory cells to sites of an antigen deposition. In some circumstances C3a and C5a can induce anaphylactic shock.
Coagulation system
collection of enzymes in the blood plasma whose activity forms blood clots. The coagulation system is activated by damage to blood vessels.
Kinin system
enzymatic cascade of plasma proteins that is triggered by tissue damage and helps facilitate wound healing
Protease inhibitors
small proteins such as the serpins that can bind to proteases and inhibit their enzymatic activity
Defensins
family of antimicrobial peptides 35-40 amino acids long that can penetrate microbial membranes and disrupt their integrity
(Alpha & beta defensins)
Subset of the secreted antimicrobial peptides called defensins
Cryptidins
alpha defensins HD5 and HD6, which are antibacterial proteins secreted by the Paneth cells of the small intestine.
Lectins
receptors and plasma proteins that recognize carbohydrates
Mannose receptor
cell surface receptor on dendritic cells, macrophages, and other leukocytes that binds to mannose residues on the surface of pathogens
Glucan receptor
receptor on the surface of macrophages and neutrophils that recognize microbial carbohydrates.
Scavenger receptor
phagocytic receptor of macrophages that binds to an assortment of negatively charged ligands, including sulfated polysaccharides, nucleic acids, and the phosphate-containing lipoteichoic acids in the cell walls of gram positive bacteria
Lipopolysaccharide (LPS)
an alternative term for bacterial lipopolysaccharide; (LPS) component of the surface of gram negative bacteria that activates toll receptors on macrophages and other leukocytes as part of the innate immune response.
Receptor-mediated endocytosis
Internalization of extracellular material that is bound to a receptor at the cell surface
Endosome
intracellular membrane bounded vesicle that is formed by the invagination and pinching off of a portion of plasma membrane. It contains extracellular material
Phagosome
intracellular vesicle containing material taken up by phagocytosis
Lysosomes
digestive intracellular organelle that contains degradative enzymes and breaks down macromolecules
Phagolysosomes
intracellular vesicle formed by fusion of a phagosome with a lysosome, in which the phagocytosed material is broken down by degradative lysosomal enzymes
Cytokines
proteins made by cells that affect the behavior of other cells. Cytokines made by lymphocytes are often called lymphokines or interleukins (abbreviated IL). Cytokines bind to specific receptors on their target cells.
Toll like receptors (TLRs)
class of receptors of innate immunity that are present in many types of leukocytes, especially macrophages, dendritic cells, and neutrophils. Each type of TLR is specific for a different type of common pathogen component, such as bacterial lipopolysaccharide or other cell wall components. The responses of macrophages and dendritic cells to stimulation via TLRs are also essential to enabling the initiation of an adaptive immune response.
Inflammatory cytokines
cytokines that promote inflammation
