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Immunology and Microbiology > induced innate immunity (exam 2) > Flashcards

induced innate immunity (exam 2) Flashcards

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Biology 101 flashcards
1
Q

induced innate immunity

A

4hrs to 4 days after infection
new DNA transcription and protein synthesis

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2
Q

induced innate immunity involves the

A

recruitment of soluble effector molecules and effector cells to infected tissue

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3
Q

what is involved in the induced innate immune response?

A

resident effector cells
internal signaling
external signaling
recruited effector cells
induced complement pathways

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4
Q

internal signaling in induced leads to

A

gene expression changes

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5
Q

external signaling in induced leads to

A

cytokine production

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6
Q

PAMP

A

pathogen associated molecular pattern

structural feature on microbe surface

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7
Q

PRR

A

pattern recognition receptor

molecule on immune cell surface that recognizes and binds PAMPS
distinguish between self, non self and altered self

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8
Q

many microbial ligands are

A

carbohydrates and lipids not present on eukaryotic cells

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9
Q

receptors for microbial ligands

A

lectins
scavenger receptor
CR3, CR4

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10
Q

lectins

A

recognize carbohydrates

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11
Q

scavenger receptor

A

binds negatively charged ligands
including apoptotic human cells

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12
Q

CR3 and CR4

A

bind complement and microbial agents

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13
Q

binding of CR3 and CR4 triggers

A

receptor mediated endocytosis

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14
Q

other macrophage receptors

A

trigger cytokine release

Toll-like receptor, NOD-like receptor, RLR

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15
Q

Toll like receptor

A

several types, each specific for common elements of different microbial products

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16
Q

TLR4

A

recognizes LPS and other molecules on gram NEGATIVE bacteria
generates intracellular signals through cytoplasmic domain –> causes gene expression

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17
Q

TLR4 causes gene expression that triggers

A

induced innate immune responses and inflammation (inflammatory cytokines)

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18
Q

2 major types of Toll like receptors

A
  1. plasma membrane bound
  2. endosomal membrane bound
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19
Q

plasma membrane bound TLR

A

direct contact with EXTRACELLULAR pathogen

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20
Q

endosomal membrane bound TLR

A

sense mostly viral DNA and RNA (INTRACELLULAR)
released in extracellular environment and taken up by cells

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21
Q

When discussing TLR receptors, if there is an intracellular pathogen versus an extracellular pathogen you can expect

A

a different response since different receptors are triggered

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22
Q

NF-kB pathway

A

major role in innate and adaptive response

activation of nuclear factor kB –> antigen binding –> activation and nuclear translocation of NFkB into nucleus –> activates expression of genes –> inflammation

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23
Q

NEMO deficiency

A

genetic lack of IKK subunit
susceptible to bacterial infections

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24
Q

interferon pathway

A

response to viral infections, intracellular bacteria
IRF7/IRF3

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25
Q

IRF7 or IRF3 results in

A

synthesis and secretion of type 1 interferons –> infected cells will be killed

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26
Q

with TLR signaling, cells of the innate immune response can _____________ to different typers of _________

A

tailor response

pathogens

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27
Q

TLR response to extracellular bacteria

A

inflammatory cytokines

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28
Q

TLR response to viral

A

interferons

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29
Q

NOD-like receptors

A

recognize parts of cell wall from phagocytose bacteria

production of inflammatory cytokines

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30
Q

RIG-1 like receptors

A

recognize viral RNA

production of type 1 interferons

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31
Q

cytokines

A

small signaling proteins made in response to external stimuli

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32
Q

pro inflammatory cytokines secreted by MO

A

IL-1b
TNF-a
IL-6
IL-12
CXCL8 and CCL2

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33
Q

master regulator of inflammation

A

IL-1b

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34
Q

IL-12 induces

A

NK lymphocyte proliferation

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35
Q

chemokines

A

small proteins that attract specific leukocytes

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36
Q

chemokine follow a

A

concentration gradient (low to high)

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37
Q

chemokine recruit

A

neutrophil and monocytes to alter cell adhesive properties and guide neutrophils/monocytes along gradient

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38
Q

IL-1 inhibitors approved for clinical use

A

anakinra - IL-1 antagonist
canakinumab - neutralizes IL-1b
rilonacept - neutralizes IL-1a/IL-1b

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39
Q

at the site of infection, activated ___________ secrete __________

A

resident macrophages

inflammatory cytokines

40
Q

TNF-a

A

stimulates vascular endothelial cells to make platelet activating factor

triggers bloot clotting

41
Q

systemic infection

A

pathogen is disseminated throughout the body via bloodstream

42
Q

septic shock

A

widespread clotting in capillaries, organ failure

43
Q

people with a defective TLR

A

are at increased risk for septic shock
widespread TNF-a production

44
Q

phagocytic cells

A

macrophages and neutrophils

45
Q

macrophages

A

long lived
reside in tissues
immediate response
phagocytosis

46
Q

neutrophils

A

short lived
circulate in blood
recruited by macrophages

47
Q

neutrophils

A

granulocytes
polymorphonuclear leukocytes
short life span, constantly made in bone marrow

48
Q

how many neutrophils enter the mouth and throat each day?

A

3x10^9

49
Q

_________ of neutrophils is the first step in inflammatory response

A

arrival

50
Q

neutrophils die within

A

hours of entry into tissue

(this is why pus is at infected wounds)

51
Q

neutrophils have

A

surface receptors for inflammatory mediators

52
Q

ligand/receptor interactions (for neutrophils) induce

A

expression of adhesion molecule

expression of ligands for adhesion molecules on vascular endothelial cells in capillaries near infection

53
Q

extravasation

A

migration from vessel to tissue

54
Q

steps of extravasation of neutrophils

A
  1. neutrophil is slowed down by VEC
  2. tight binding
  3. diapedesis
  4. migration to center of infection in tissue
55
Q

tight binding step of extravasation

A

weak interactions, chemokines induce stronger ones

neutrophil stops rolling

56
Q

diapedesis step of extravasation

A

neutrophil squeezes between adjacent VEC and reaches basement membrane

57
Q

migration to center of infection in tissue (extravasation)

A

driven by gradient (CXCL8)

58
Q

homing

A

all WBCs leave the blood and migrate to infected tissue

59
Q

what determines where and when homing occurs?

A

cytokines and chemokines

60
Q

target identification of neutrophils on pathogens

A

phagocytic receptors for microbial products
complement receptors for opsonized microbes

61
Q

NADPH oxidase

A

produces superoxide radicals consuming O2 which removes H ions and produces hydrogen peroxide

62
Q

fusion of phagosomes with neutrophil granules

A

NADPH oxidase raises pH of phagosome activating antimicrobial peptides

63
Q

fusion of phagosome with lysosomes (neutrophils)

A

acid hydrolases finish the job, then the neutrophil dies

64
Q

chronic granulomatous disease

A

defect in NADPH oxidase
no respiratory burst
leads to chronic bacterial/fungal infections

65
Q

neutrophil extracellular traps

A

trap and kill pathogens

66
Q

systemic effects of inflammatory cytokines in innate immunity

A

induce fever
produce acute-phase response

67
Q

induce fever

A

act on hypothalamus and muscle
fat cells generate heat
helps fight infections

68
Q

name of molecules that induce fever

A

pyrogens

69
Q

acute phase proteins

A

change spectrum of soluble plasma proteins made by liver cells

70
Q

mannose binding lectin

A

binds carbohydrates of bacteria, viruses, fungi, protozoans
triggers lectin pathway

71
Q

how does mannose binding lectin not attach to human cells?

A

it can attach only to repetitive structures on pathogens

72
Q

C reactive protein (CRP)

A

binds phosphocholine of bacterial and fungal cell walls
triggers classical pathway in absence of antibody

73
Q

serum amyloid A protein

A

induces inflammatory cytokine production in macrophages

74
Q

fibrinogen

A

blood clotting
localizes pathogen and prevents spread

75
Q

lectin pathway

A

binding of MBL to bacterial surface
cleaves C4 and C2

76
Q

genetic deficient in MBL

A

can result in severe meningitis
common

77
Q

classical pathway

A

binding of C1 to C reactive protein on pathogen activates protease
cleaves C4 and C2 –> opsonization

78
Q

which pathways of complement need to be induced

A

lectin and classical

79
Q

the main complement pathway at the start of infection

A

alternative

80
Q

type 1 interferons

A

made by any human cell infected with virus
interfere with viral replication

81
Q

how do type 1 interferons alert the area that there in an infection?

A

they signal neighboring cells to prepare
alert immune cells
make virus infected cells targets for NK cells

82
Q

forms of type 1 interferons

A

IFN-b and IFN-a

83
Q

synthesis of interferons is induced by

A

viral infection or binding to a signaling receptor since dsRNA is not found in healthy human cells

84
Q

what type of fashions can interferons act in?

A

paracrine and autocrine

85
Q

interferon response

A

induce resistance to viral replication in all cells
increase expansion of ligands for receptors on NK cells
activate NK cells to kill virus infected cells

86
Q

plasmacytoid dendritic cell

A

produces huge amounts of type 1 interferon
found in blood and lymphoid tissue

87
Q

NK cells

A

5-25% of lymphocytes
against intracellular infections
migrate from blood to tissue in response to inflammatory cytokines

88
Q

functions of NK cells

A

kill infected cells (stimulated by IFN-a,b)
produce cytokines (stimulated by IL-12)

89
Q

what type of cytokine does NK cells produce?

A

IFN-g which activates macrophages

90
Q

NK cells interact with

A

dendritic cells

suppress or activate them depending on sufficiency of innate response

91
Q

how do NK cells kill infected human cells?

A

inducing them to die via apoptosis

92
Q

ligands on NK cells

A

inhibitory and activating receptors

93
Q

type of ligands on healthy cells

A

more inhibitory over activating

94
Q

when NK cells are ________ they outnumber dendritic cells and _______ the dendritic cells

A

abundant

kill

95
Q

when NK cells are scarce, they signal the dendritic cells and

A

initiate the adaptive immune response

Immunology and Microbiology (22 decks)

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