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Biol 389-Immuno > Chapter 2 > Flashcards

Chapter 2 Flashcards

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
Q

TRIF

A

toll-receptor-associated activator of interferon

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26
Q

TRAM

A

toll-receptor associated molecule

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27
Q

phagocytosis by macrophages

A

facilitated by opsonin receptors (complement receptors)

28
Q

inflammation by macrophages

A

TLR signaling activating transcription factor NFkB which induces production of inflammatory cytokines

29
Q

IL1 and TNF-alpha

A

induce fever and increase vascular permeability

30
Q

IL6

A

induces fever and activates liver cells to produce acute phase response proteins

31
Q

CXCL8

A

chemokine attracts neutrophils and basophils

32
Q

IL12

A

recruits and activates NK cells

33
Q

inflammasome

A

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
Q

NLRPs

A

NOD-like receptor proteins

35
Q

ASC

A

apoptosis-associated speck-like protein containing a CARD domain

36
Q

neutrophil functions

A

peripheral circulation
fast turnover

37
Q

extravasation

A

neutrophils exit blood circulation via extravasation to sites of infection and inflammation

38
Q

extravasation

A

neutrophils exit blood circulation via extravasation to sites of infection and inflammation
requires adhesion molecule interactions

39
Q

glycoproteins

A

on neutrophils surface
bind to selectins on vascular endothelial cell surface

40
Q

integrin

A

on neutrophil surface
bind to ICAM on vascular endothelial cell surface

41
Q

extravasation steps

A

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
Q

diapadesis

A

neutrophils cross to endothelial cell layer

43
Q

migration

A

chemotaxis of neutrophils towards source of CXCL8

44
Q

effector mechanisms

A

fusion of phagosome with granules containing proteases and antimicrobial proteins/peptides
respiratory burst
NETs (neutrophil extracellular traps)

45
Q

respiratory burst

A

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
Q

Type 1 interferons, IFN-alpha and IFN-beta

A

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
Q

inhibitory receptors

A

bind cell surface proteins present in all healthy cells that present peptide fragments from inside the cell
set to kill by default

48
Q

activating receptors

A

NKG2D binds MIC-A and MIC-B which are expressed in response to cellular stress
stop making self marker

49
Q

receptor types

A

Killer-cell immunoglobulin-like receptors (KIR)
lectin-like receptors

50
Q

NK cell killing mechanism

A

look for cells lacking inhibitors
release granule contents of perforin and granzymes towards the altered cells to initiate apoptosis

51
Q

dendritic cells

A

phagocytose pathogens and transport to lymph nodes
process and present pathogen protein fragments to T cells
pattern recognition

52
Q

NK cells

A

once activated, secrete IFN-gamme which recruits cytotoxic T cells

53
Q

systemic infection

A

infection spreading through bloodstream

54
Q

systemic infection

A

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
Q

malfunction in TLR

A

causes lack of cytokine production
leads to greater susceptibility to infection

56
Q

malfunction in innate cell function

A

defective macrophage can lead to persistence of infection
defective neutrophil function leads to granulomas
defective NK cells cause chronic and recurrent viral infections

57
Q

granulomas

A

fused macrophages attempting to clear infected neutrophils

58
Q

What term refers to the process where neutrophils leave circulation and enter tissues?

A

diapedesis

59
Q

Which is the most important transcription factor for responding to LPS?

A

NFkB

60
Q

What type of action do most cytokines produce?

A

paracrine

61
Q

IL-1 is activated by the action of what protein?

A

caspase-1

62
Q

Which is NOT true of the innate immune system?

A

it has no memory
it is activates 7-10 days later

63
Q

What does TLR-4 primarily recognize?

A

Lipopolysaccharide

64
Q

RIG-1 is a cytosolic receptor that binds to what?

A

Viral RNA

65
Q

What is our immune system’s first line of defense?

A

skin

66
Q

Which cytokines is secreted in response to viral infection?

A

Interferon

67
Q

During the oxidative burst, what reactive oxygen species is produced by NADPH oxidase?

A

superoxide

Biol 389-Immuno (5 decks)

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