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BIO 3382 - Exam 1 - Chapter 2 Vocabulary

Terms in this set (148)

Extracellular
Infections that occur in the space between human cells where pathogens are accessible to soluble molecules of the immune system
Intracellular
Infections that occur when pathogens replicate inside human cells; Pathogens in nucleus or cytoplasm can be destroyed by killing the infected cell; They can also stimulate activity of the cell to increase microbial activity
Complement
Soluble proteins made by the liver that coat bacteria and viruses to facilitate identification and phagocytosis
Liver
Organ that makes complement proteins
Blood, Lymph, Extracellular Fluids
Three places where complement is present
Proteases
Highly specific proteolytic enzymes that are components of complement and are involved in infection and activation of pathway enzymes leading to complement cleavage and activation
Zymogens
Inactive proteases that are non-cleaved
C3 (Complement Component 3)
Most important protein of the complement system
C3a
Chemoattractant for effector cells; Smaller fragment of cleaved C3
C3b
Larger fragment of cleaved C3 that bonds to the pathogen's surface and tags the pathogen for phagocytosis by organizing proteins that can damage the pathogen's membrane and is used to make more C3 convertase
Complement Fixation
The binding of a complement component to the pathogen's surface
Alternative
Pathway of complement activation that beings working at the start of an infection
Lectin
Pathway of complement activation that is induced by infection and is activated by a complex of MBL that opsonizes update to monocytes
Classical
Pathway of complement activation that requires binding of antibody or C-reactive protein to pathogen's surface
iC3
Formed when the thioester bond of some C3 molecules is hydrolyzed
Factor B
Inactive complement that binds to iC3 and C3b and is cleaved by Factor D
Factor D
Protease that cleaves Factor B bound to C3
Ba
Fragment of cleaved Factor B that is released after cleavage
Bb
Fragment of cleaved Factor B that remains bound to the complex
C3 Amplification
Occurs when C3b molecules fix to the pathogen and leads to production of more convertase so that the pathogen becomes coated rapidly
C3bBb
A powerful C3 convertase called the alternative C3 convertase that binds C3 and cleaves it into C3b
Properdin (Factor P)
Regulatory protein that is plasma located and binds to C3bBb and stabilizes the connection to the pathogen surface
Factor H
Regulatory protein that is plasma located and binds to C3b and cleaves it to iC3b with cofactor I
Factor I
Cofactor to Factor H in the cleavage of C3b into iC3b; Also cleaves C3b after C3bBb complex is bound by MCP and Bb is dissociated
Properdin, Factor H
The two plasma located regulatory proteins that determine the extent and site of C3b deposition
DAF (Decay-Accelerating Factor)
Membrane located regulatory protein that binds to the C3b component of C3bBb and causes Bb to dissociate and the complex to inactivate
MCP (Membrane Co-Factor Protein)
Membrane located regulatory protein that binds to the C3b component of C3bBb and causes Bb to dissociate and causes Factor I to cleave and inactivate the complex to iC3b
Sialic Acid
Substance that is found on the surfaces of S. pyrogenes and S. aureus that binds to Factor H so that any C3b that contacts the Factor H is inactivated (form of Bacterial Adaptation)
Macrophages
Long-lived cells that participate in innate and adaptive immunity; Mature form of circulating monocytes that take up residence in tissue
Macrophages
The first effector cells to attack when pathogens invade tissue; Found in connective tissue, lining of GI and respiratory tracts, alveoli of lungs and liver
Kupffer Cells
Macrophages found in the liver
CR1 (Complement Receptor 1)
Receptor site on macrophages that bind C3b fragments that are bound to microbial surface; Leads to opsonization and stops C3 convertase from carrying out amplification and allows C3b to be cleaved by Factor I so that it is incapable of amplification
Opsonization
The process of coating a pathogen that enhances the attachment and thus the efficiency of the phagocytic action
CR3, CR4
Receptor sites of macrophages that bind iC3b fragments on microbial surfaces (do not have the ability to facilitate phagocytosis)
C5, C6, C7, C8, C9
Five complement components that are involved in the cascade response (MAC)
Alternative C3 Convertase
Formed when C3b binds to C3bBb
Alternative C5 Convertase
Enzyme produced when C3b binds to C3bBb and cleaves the C5 component into C5a and C5b
MAC (Membrane Attack Complex)
Complex that is built from the C5-C9 complement components that is capable of penetrating pathogen membranes by initiating polymerization of C9 which forms transmembrane proteins
C6
Complement component that binds to C5b but does not anchor into the lipid bilayer
C7
Complement component that binds to C5b and anchors into the hydrophobic portion of the lipid bilayer - relatively shallow (involved in MAC attack)
C8
Complement component that binds to C5b complex exposing the hydrophobic site that is inserted into the bilayer which causes polymerization of C9 (involved in MAC attack)
C9
Complement component that is polymerized to create a pore in the pathogen membrane (involved in MAC attack)
S Protein, Clusterin, Factor J
Three soluble proteins that prevent C5, C6, and C7 from associated with the membrane of host cells to protect them from invasive action
HRF, CD59
Two proteins that function to deter the C9 attachment and polymerization to host cells to protect them from invasive action
Lipid Tails
Structure that link protective proteins to a host cell
C3a, C5a
Complement component fragments that increase inflammation at the site by binding to receptors on cells; Can induce anaphylactic shock
Phagocytes, Endothelial Cells, Mast Cells
Three cells that have receptors for C3a and C5a
Anaphylactic Shock
Inflammation in tissues throughout the body that can be induced by C3a and C5a
Anaphylatoxins
Term used for C3a and C5a because they can induce contractions of smooth muscle, induce degranulation of mast cells and basophils which ultimately allows plasma proteins and cells to pass out of blood and to the site of infection easily
C5a
Complement component fragment that affects neutrophils and monocytes by increasing their adherence to blood vessels, directing them towards areas where complement is being fixed, increasing their capacity for phagocytosis, and raising expression of CR1 and CR3 receptor sites
C5a
The more stable and more potent of the two anaphylatoxins
Coagulation System
Series of plasma enzymes that form blood clots to stop organisms from entering blood and lymph and reduce blood/fluid loss; Activated when blood vessels are damaged
Kinin System
Series of enzymatic plasma proteins triggered by tissue damage that causes vasodilation to increase cellular material exchange of innate immunity; Causes smooth muscle relaxation, edema, and pain; Interacts with clotting cascade, fibrinolytic cascade, and complement cascade
Protease Inhibitors
Function to break down human tissue, aid in pathogen dispersal, and inactivate antimicrobial proteins; Found in human secretions and plasma
alpha2 macroglobulin
A protease inhibitor that stops attack of substrates
alpha
Defensins that are expressed by neutrophils and Paneth cells of the small intestine
HD5, HD6
Two alpha-defensins (cryptdins) from Paneth cells
Cryptdins
Alpha-defensins from Paneth cells (HD5 and HD6)
Beta
Defensins expressed by many epithelial cells, incuding skin, respiratory and urogenital tracts that kill enteric pathogens, but maintain normal gut flora
Lectins
Macrophage receptors and plasma proteins that recognize carbohydrates (examples are mannose receptor and glucan receptor)
Mannose Receptor, Glucan Receptor
Two examples of lectins
Scavenger
Macrophage receptor that binds to negatively charged ligands such as sulfated polysaccharides, nucleic acids, and lipoteichoic acids
CR3, CR4
Macrophage receptors that recognize iC3b ligan and other microbial products such as bacterial lipopolysaccharide (LPS), found in Gram negative bacteria
Receptor-Mediated Endocytosis
Occurs when microbial ligands bind to macrophage receptors where the pathogen is surrounded by the macrophage membrane and is taken into an endosome (phagosome) that fuses with a lysosome and uses enzymes and toxic substances to destroy the pathogen
Endosome (Phagosome)
The vesicle of a macrophage in which the pathogen is surrounded by; Merges with lysosomes
Phagolysosome
Formed when a phagosome fuses with a lysosome; Full of enzymes and toxic substances that destroy the pathogen
Toll-Like Receptors (TLRs)
Signaling receptors that are each specific for different microbial products
TLR4
TLR that is expressed by macrophages and target LPS on Gram negative bacterial; Signals the release of inflammatory cytokines which induce inflammation at the site of infection
Transmembrane Protein, Cytoplasmic Signaling Domain
Two components of TLRs
Transmembrane Protein
Component of TLRs that functions for pathogen recognition; made of leucine-rich repeating regions (LRRs)
LRRs (Leucine-Rich Repeating Units)
Make up the transmembrane protein of TLRs; Varying numbers account for different binding specificity
LPS
Binds to TLR4, MD2, and CD14 on macrophage surface in TLR pathway 1
TIR domain
Binds to protein MyD88 in TLR pathway 1
TLR4, MD2, CD14
Three molecules on the macrophage surface that bind to LPS in TLR pathway 1
MyD88
Bridge protein that binds to TIR domain and IRAK 4 in TLR pathway 1
IRAK4
Protein kinase that binds to MyD88 and phosphorylates TRAF6 in TLR pathway 1
TRAF6
Adapter protein that is phosphorylated by IRAK4 in TLR pathway 1
Kinase Cascade
Activates IKK in TLR pathway 1
IKK
Inhibitor kinase that is activated by kinase cascade and phosphorylates IkB in TLR pathway 1
IkB
Phosphorylated by IKK and releases NFkB in TLR pathway 1
NFkB
Released by IkB and enter the nucleus and activates genes encoding inflammatory cytokines in TLR pathway 1
NEMO Deficiency
A rare genetic disorder where patients are missing a subunit from IKK; NFkB activation is impaired because macrophage activation through TLR4 is inefficient; Also involves deep-set eyes, sparse hair, conical/missing teeth; More common in boys (on X-Chromosome)
Pathway 1
TLR pathway that describes how cytokine release is signaled from the pathogen recognition
Pathway 2
TLR pathway that describes how TLR3/TLR4 responds to viral infections
TRIF, TRAM
Adapter proteins that form a complex with TLR3 or TLR4 in TLR pathway 2
TRAF3
Phosphorylated and leads to a kinase cascade in TLR pathway 2
IRF3
Phosphorylated then enter the nucleus to direct the transcription of Type I interferons in the TLR pathway 2
Type I Interferons
Cytokines that respond to viruses and intracellular bacteria
Inflammation
Local accumulation of fluid causing swelling, reddening, and pain
Chemokine
A chemoattractant cytokine
CXCL8
A chemokine that attracts leukocytes two ways; Recruit neutrophils from blood into infected area
Chemokines
Binding effects leukocytes by changing the cell's adhesive properties so it can leave blood and enter tissue and guides movement of the cell along a gradient in solution and on surfaces of tissue
IL-12
Chemokine that activates natural killer lymphocytes of innate immunity which specialize in viral defense
IL-1, TNF-alpha
(2) Chemokines that facilitate movement of neutrophils, NK cells and other effector cells into infected areas
Inflammatory Mediators
Molecules involved in the induction of inflammation
Septic Shock
Condition in which systematic bacterial infection induces macrophages in several areas of the body to release TNF-alpha; Blood vessels dilate and fluids leak into the tissue, can cause massive blood clotting (that can cause organ failure due to lack of blood supply)
Gram Negative
Bacteria that are the most common cause of septic shock
Phagocytic Cells
The primary method to destroy invading pathogens
Macrophages, Neutrophils
Two types of phagocytic cells
Pyogenic
Bacteria that induce pus
Adhesion Molecules
Interact to provide movement of leukocytes between blood and tissue
Selectins, Mucins, Integrins, Immunoglobulins
Four types of adhesion molecules
Selectins
Carbohydrate binding proteins (lectins) specific for vascular addressins (adhesion molecules)
Integrins
Large family of adhesion molecules that includes CR3 and CR4; Ligands are for proteins
Extravasation
Process by which neutrophils leave blood and enter tissue
P-selectin, E-selectin
Activated when neutrophils interact with blood vessel walls; Bind with the leukocyte's surface and roll it along the vascular endothelial surface
Integrins
Molecules that are present on the neutrophil and change structure upon exposure to cytokines from the inflamed tissue to strengthen adhesion to the endothelium so the neutrophil stops rolling
Diapedesis
Process by which the leukocyte crosses between endothelial cells to reach the basement membrane
Homing
Process by which white blood cells leave the blood and migrate to tissue
Rolling Adhesion - Tight Binding - Diapedesis - Migration
Four steps (in order) of extravasion
Microbicidal Substances
Stored in the granules of neutrophils
Azurophilic, Specific
Two types of neutrophil granules
Azurophilic (Primary)
Neutrophil granules that are packed with proteins and peptides to disrupt and digest microbes (examples are lysosome, defensins, and cathepsin G)
Specific (Secondary)
Neutrophil granules that contain unsaturated lactoferrin and NADPH oxidase
Lactoferrin
Component of specific granules that competes with microbes for iron and copper
NADPH Oxidase
Component of specific granules that causes the pH inside of the phagosome to increase so proteins are activated to attack pathogens
Respiratory Burst
Provides the power for neutrophil attacks by a brief increase in oxygen consumption
Apoptosis
Result when neutrophil granules are used up
Macrophage
Phagocytizes a dead neutrophil
Fever
The systemic response of a rise in body temperature caused by the inflammatory cytokines IL-1, IL-6, and TNF-alpha
Hypothalamus
Site of temperature control sites that cytokines act upon during fever
Pyrogens
Molecules that induce fever
Exogenous
Pyrogens that originate from outside the body (bacterial products); Induce cytokines which cause fever
MBL, CRP
Two acute-phase proteins that enhance complement fixation at pathogen surfaces
MBL (Mannose-Binding Lectin)
Acute-phase protein that has a flower-like binding structure with multiple points of attachment (member of family of collectins)
CRP (C-Reactive Protein)
Acute-phase protein that has 5-identical subunits (pentamer) and triggers the classical pathway
Acute-Phase
Proteins that bind to structure on bacteria not found in human cells and act as opsonsins, activate complement, and facilitate phagocytosis
MBL
Circulates in plasma in association with MASP-1 and MASP-2
MASP-1, MASP-2
Two protease molecules that associate with MBL
MASP-2
In the lectin pathway, binds and cleaves C4 into C4b and C4a fragments
C4b
In the lectin pathway, binds to the microbial surface
C2
In the lectin pathway, binds to the activated MASP-2 of the MBL complex; Cleaved by MASP-2
MASP-2
In the lectin pathway, cleaves C2
C2a
In the lectin pathway, binds to C4b to form C4b2a, classical C3 convertase
C4bC2a
In the lectin pathway, binds and cleaves C3
MBL Binding, Activation of C4 & C2, MASP proteins
(3) Unique features of the lectin pathway
10%
Approximate percentage of the population that has non-functional variants of MBL
C-Reactive Protein
Binds to bacterial surface to begin the classical pathway of complement activation
C1
In the classical pathway, bound by c-reactive protein
C1q
In the classical pathway, binds pathogens
C1r, C1s
In the classical pathway, activates C2 and C4
C2, C4
In the classical pathway, activated by C1r and C1s
Isotypes
Types of type I interferons
Interferon Response
Changes that occur as genetic expression as a result of the binding of interferon to its receptor
Interferon-Producing Cells (IPCs)
Cells that secrete up to 1000x more interferon than other human cells
Plasmacytoid Dendritic Cells
A dendritic cell that can still produce interferon
IFN-gamma
Activates macrophages to secrete cytokines to activate T-cells (initiating adaptive immune response)
NK cells
Primary source of IFN-gamma in early infection
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