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Biol 389-Immuno > Chapter 2 > Flashcards

Chapter 2 Flashcards

(67 cards)

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1
Q

physical barriers

A

skin, prevents entry
cells, line digestive tract and airways
tight junctions prevent microbes from entering
fluid secretion (mucus) remove microbe

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2
Q

chemical barriers

A

acidic pH
antimicrobial proteins
antimicrobial peptides
complement system

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3
Q

lysozyme

A

digests bacterial cell wall

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4
Q

phagocytes

A

have cell surface receptors that recognize either an opsonin or molecular pattern or pathogen surface
recruit macrophages and neutrophils

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5
Q

phagosome

A

membrane enclosed cluster of receptors binding to pathogen inducing ingestion of pathogens

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6
Q

phagolysosome

A

phagosome fusion with lysosome
low pH and digestive enzyme for destruction and degradation of pathogen

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7
Q

pattern recognition receptors (PRPs)

A

innate immune cells that recognize potential pathogens with receptors that recognize pathogen-associated molecular patterns (PAMPs)

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8
Q

pattern-associated molecular patterns (PAMPs)

A

molecules that are characteristic of a broad range of microbes not normally present in the body

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9
Q

toll-like receptors

A

recognize pattern
transmembrane proteins on cell surface and endosomes

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10
Q

lectin receptors

A

sugars
bind carbohydrates common to pathogen cell surface
binding activates phagocytosis

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11
Q

scavenger receptors

A

cell debris
bind negatively charged ligands
binding activates phagocytosis

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12
Q

cytosolic innate receptors

A

signals within cytoplasm
viruses

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13
Q

opsonin receptors

A

complement system
CR3 and CR4 receptors bind proteins bound to microbial cell surface
binding triggers phagocytosis

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14
Q

lipopolysaccharide

A

gram negative bacteria
TLR 4

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15
Q

cell signaling

A

receptor clustering triggering intracellular signaling pathways
changes in gene expression

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16
Q

cytokines

A

secreted proteins that have signaling roles in the immune system
heat, pain, swelling, redness

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17
Q

chemokines

A

a cytokine that acts as a chemoattractant for immune cells
bread crumbs for immune cells to come to site of infection

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18
Q

antiviral cytokines

A

Interleukin (IL)-12
interferon-alpha and -beta
activate NK cells

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19
Q

interferons

A

warn neighbors
antiviral proteins secreted making it harder to spread

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20
Q

Toll-Interleukin receptor (TIR)

A

domain of TLRs with a cytosolic signal

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21
Q

factor NFkB

A

a transcription factor TLRs recognize by bacterial PAMPs via signaling cascade starting with myD88

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22
Q

TLRs binding extracellular PAMPS activating NFkB

A

TLR4 activated by LPS
converted to TIR

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23
Q

TLR that bind viral nucleic acids activate IRF3 and IRF7

A

ligand bind cause TRIF and TRAM to bind TIR region

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24
Q

TLR that bind viral nucleic acids activate IRF3 and IRF7

A

ligand bind cause TRIF and TRAM to bind TIR region
TRIF and TRAM activate TRAF3
TRAF3 phosphorylate and activates IRF3 and IRF7
phosphorylated IRF3 and IRF7 enter nucleus, promote defense

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25
TRIF
toll-receptor-associated activator of interferon
26
TRAM
toll-receptor associated molecule
27
phagocytosis by macrophages
facilitated by opsonin receptors (complement receptors)
28
inflammation by macrophages
TLR signaling activating transcription factor NFkB which induces production of inflammatory cytokines
29
IL1 and TNF-alpha
induce fever and increase vascular permeability
30
IL6
induces fever and activates liver cells to produce acute phase response proteins
31
CXCL8
chemokine attracts neutrophils and basophils
32
IL12
recruits and activates NK cells
33
inflammasome
IL1 produced as pro-IL-1 IL1 activation requires activation of Caspase 1 complex of innate cytosolic receptors of NLRPs and ASC NLRPS activate Caspase 1 to cleave pro-IL-1 and generate IL1
34
NLRPs
NOD-like receptor proteins
35
ASC
apoptosis-associated speck-like protein containing a CARD domain
36
neutrophil functions
peripheral circulation fast turnover
37
extravasation
neutrophils exit blood circulation via extravasation to sites of infection and inflammation
38
extravasation
neutrophils exit blood circulation via extravasation to sites of infection and inflammation requires adhesion molecule interactions
39
glycoproteins
on neutrophils surface bind to selectins on vascular endothelial cell surface
40
integrin
on neutrophil surface bind to ICAM on vascular endothelial cell surface
41
extravasation steps
rolling adhesion via weak interaction between neutrophils and glycoproteins and selectins on endothelial cells tight binding of neutrophil integrin LFA1 to ICAM1 in response to chemokine CXCL8
42
diapadesis
neutrophils cross to endothelial cell layer
43
migration
chemotaxis of neutrophils towards source of CXCL8
44
effector mechanisms
fusion of phagosome with granules containing proteases and antimicrobial proteins/peptides respiratory burst NETs (neutrophil extracellular traps)
45
respiratory burst
activation of NADH oxidase in phagosomes consumes oxygen and generates superoxide radicals superoxide dismutase and catalase convert superoxide radicals to water and oxygen gas
46
Type 1 interferons, IFN-alpha and IFN-beta
induced in virus infected cells by activation of endosomal TLRs and cytosolic innate receptors induce NK proliferation activate protein kinase R to inhibit protein syn induce RNase L induce p53 to trigger apoptosis induce expression of cell surface proteins that signal viral infection to NK cells
47
inhibitory receptors
bind cell surface proteins present in all healthy cells that present peptide fragments from inside the cell set to kill by default
48
activating receptors
NKG2D binds MIC-A and MIC-B which are expressed in response to cellular stress stop making self marker
49
receptor types
Killer-cell immunoglobulin-like receptors (KIR) lectin-like receptors
50
NK cell killing mechanism
look for cells lacking inhibitors release granule contents of perforin and granzymes towards the altered cells to initiate apoptosis
51
dendritic cells
phagocytose pathogens and transport to lymph nodes process and present pathogen protein fragments to T cells pattern recognition
52
NK cells
once activated, secrete IFN-gamme which recruits cytotoxic T cells
53
systemic infection
infection spreading through bloodstream
54
systemic infection
infection spreading through the bloodstream TNF-alpha causes vasodilation rapid loss of blood pressure causing septic shock causing organ failure of kidneys, liver, heart and lungs
55
malfunction in TLR
causes lack of cytokine production leads to greater susceptibility to infection
56
malfunction in innate cell function
defective macrophage can lead to persistence of infection defective neutrophil function leads to granulomas defective NK cells cause chronic and recurrent viral infections
57
granulomas
fused macrophages attempting to clear infected neutrophils
58
What term refers to the process where neutrophils leave circulation and enter tissues?
diapedesis
59
Which is the most important transcription factor for responding to LPS?
NFkB
60
What type of action do most cytokines produce?
paracrine
61
IL-1 is activated by the action of what protein?
caspase-1
62
Which is NOT true of the innate immune system?
it has no memory it is activates 7-10 days later
63
What does TLR-4 primarily recognize?
Lipopolysaccharide
64
RIG-1 is a cytosolic receptor that binds to what?
Viral RNA
65
What is our immune system’s first line of defense?
skin
66
Which cytokines is secreted in response to viral infection?
Interferon
67
During the oxidative burst, what reactive oxygen species is produced by NADPH oxidase?
superoxide

Biol 389-Immuno (5 decks)

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