Inflammation 4 Flashcards

1
Q

in add’n to opsinins coating phagocytes, the neutrophil can also be triggered to engulf pathogens by

A

PAMPs on pathogens bindnig to PRR

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2
Q

CR3 and CR4 are

A

complement receptors

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3
Q

CR3 and CR4 bind to

A

C3B

IC3B

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4
Q

neutrophils have two types of granules

A

auzorophilic granules

specific granules

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5
Q

contained in the granules are

A

microbial substances

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6
Q

following delivery of the granules from neutrophils to phagosome we also get delivery of

A

lysosomal contents to phagosome

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7
Q

when lysosomes fuse with phagosome forms

A

phagolysosome

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8
Q

neutrophil after phagocytosis does what

A

dies - it exhausts itself

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9
Q

if infection isn’t resolved by neutrophils the

A

monocyte → macrophage and cleans up after neutrophil

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10
Q

part of specific granuels for killing in neutrophils is what coplex

A

NADPH oxidase complex

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11
Q

superoxide is reactive and can do what

A

damage to biomoleuless

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12
Q

superoxide dismutase converts 2O2- to

A

hydrogen peroxide

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13
Q

hydrogen peroxide converted by myeloperoxidase into:

A

HOCl (bleach!)

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14
Q

oxidative killing increases O2 demand by 100x so it’s called

A

respiratory burst

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15
Q

do resting neutrophils have NADPH complex

A

no they aren’t active in terms of oxidative killing

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16
Q

what are the non-oxidative killing list of neutrophils

A

Elastase
Cathepsins/other proteinases
Collagenase
Lactoferrin

“Cathy Elatedly Lactated in Collage”

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17
Q

which is most important killing mechanism for neutrophils

A

oxidative killing

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18
Q

in individuals without ability to form NADPH disease:

A

they are totally competent in non-oxidative killing mechansm

they have recurrent bacterial infections

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19
Q

memorize table on pg

A

87

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20
Q

monocyte differentiate into what in tissue

A

macrophage

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21
Q

how do monocyte get into infected tissue

A

same way as neutrophil
rolling
tight binding
pulled through gaps

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22
Q

monocytes and macroh[ages have what on surface

A

PRR - allows them to take up opsinized material and the bacteria or other pathogens that have glycoproteins on surface

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23
Q

receptors on surface of macrophage we need to know

A

pg 90 memorize

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24
Q

Mac-1, CD11b/CD18

A

pg 90

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25
Q

Dectin-1

A

allows fungi to be recognized and taken up - it binds to beta glucans (part of fungal cell wall)

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26
Q

macrophage has how many TLR

A

10 - can detect variety of pathogens

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27
Q

what is first to infiltrate infection

A

neutrophil

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28
Q

neutrophils are mobilized from

A

bone marrow

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29
Q

neutrophils once they do their job they will

A

die

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30
Q

the cell following neutrophil will

A

continue fighting or clean up dead neutrophils

monocyte → macrophage

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31
Q

cytokines that promote inflammation

A

IL-1, IL-6, IL-8, IL-12, Interferons, TNFs (TNF-)

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32
Q

IL12 and interferons are important in what response

A

innate respose against viral infections

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33
Q

once inflammatory response has done its job need what

A

IL-10 and TGF-β

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34
Q

IL-10 and TGF-β are

A

anti-inflammatory

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35
Q

IL-1, IL-6, TNF-a control

A

acute phase response

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36
Q

IL-1, IL-6, TNF-a iportant for promoting

A

acute phaseinflammation

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37
Q

interferons do qhat

A

Activate NK cells.

Provide anti-viral protection to neighboring cells.

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38
Q

IL is a

A

cytokine

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39
Q

IL-1 induces expression of

A

adhesion molecules on vascular endothelial cells

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40
Q

TNF alpha

A

shares with IL - 1 increases expression of adhesion molecules on vascular endothelial cells
allows recuirted leukocytes to roll on endothelial cells and halt when integrin has been activated by exposre of leukocyte to chemoattractant
induces production of acute phase protiens
induces sytokine secretion by inflammatory cells

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41
Q

Tumor Necrosis Factor-alph is

A

TNF alpha

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42
Q

TNF alpha important for controling

A

localized infection

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43
Q

systemic release of infection thats bad why

A

system production of TNF alpha will cause bulk movement of fluid from circulation into tissues
will lead to dramatic drop in blood pressure, collapse of blood vessels, which leads to disseminated intravascular coagulation which leads to oran failure

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44
Q

Disseminated intravascular coagulation leads to

A

organ failure

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45
Q

release of gram negative through body can lead to

A

septic shock/death

46
Q

IL-8 signals thorugh

A

g proteins

47
Q

IL-8 acitvates

A

integrin to allow leukocyte to pull itself into tissues

48
Q

anti-inflammatory cytokines

A

IL-10

Transforming Growth Factor- (TGF-)

49
Q

chronic inflammation happens if

A

infection persists
autoimune disease
response to undigestible foreign material

50
Q

hallmark of chronic inflammtion is activation of

A

t cells

51
Q

activation of t cells promotes activation of

A

marophages

52
Q

once t cells activated they attract more

A

monocytes and activate monocytes once they differente to mcrophages via cytokine IFN-gamma

53
Q

neutrophils are secreted adn their activity associated with

A

TNF-alpha (secreted by T cells)

54
Q

CD4 T cell subset aquired for cell mediated immune resposes

A

Th1

55
Q

Th1 upregulate

A

Cytokines from a type of CD4 T cell called Th1 cells upregulate the intracellular killing ability of macrophages and promote the differentiation and activation of Cytotoxic T cells.

56
Q

Activated T cells make

A

IFN - gamma
CD40 ligand
CXCL2

57
Q

CD40 ligand will bind to

A

CD40 on what cel is interacting with

58
Q

IFN gamma and CD40 together activates

A

activates macrophages to destroy what they have taken up

59
Q

CXCL2 cause

A

macrophages to accumulate at site of infection

60
Q

granuloma

A

structure our immune system uses to wall off bacteria that we cannot eliminate - like microbacteria

61
Q

interaction b/w th1 cells and macrophages result in formation of

A

granuloma

62
Q

formation of granuloma takes

A

weeks to months

63
Q

describe granuloma

A

fuse together and form syncitia (multinucleated giant cells)

bacteria trapped in it

64
Q

what is doinant cell in granuloma

A

macrophages

tiny layer of t cells surrounding it

65
Q

dominant effector cells in acute inflammation

A

neutrophils

66
Q

dominant effector cells in chronic inflammation

A

Macrophages

Th1

67
Q

innate response against viruses, who is very important in it

A

type I IFNs

68
Q

type I IFN does what

A

primes adj cells to be much less suscpt. to promoting virus replication
induce PKR and RNase L

69
Q

Type I IFNs increase expression of

A
MHC class I
enhance the ability of affected cell to show that it is infected

APC

70
Q

cytotxoci t cells need what to recognize virally infected cell

A

MHC class I

71
Q

APC stands for

A

antigen presenting cell

72
Q

draw chart of induction of antiviral state

A

pg 108

73
Q

viral genome is coactivator for

A

oligoadentylate synthase - this will then activate RNase L

74
Q

during innate response of viral infection what is first thing you will see

A

innate cytokines being produced
type I interferon
IL-12

75
Q

in vast majority of cases the innate response is not able to

A

eliminate infection

76
Q

look at graph of virus titer with viral infection

A

pg 109

77
Q

NK cells have ability to

A

kill cells infected w/ certain viruses

78
Q

type II interferon

A

IFN gamma

79
Q

production of type II interferon is restricted to which cells

A

NK and T cells

80
Q

production of type I interferon by which cells

A

almost all cells

81
Q

IFN gamma promotes

A

killing by macrophages

pdoruction of antiviral agents by uninfected cells (RNase L, etc)

82
Q

IFN I and II increase expression of

A

MHC I

83
Q

IFN II increase expression of q

A

MHC II

84
Q

type II interferen signals through

A

jak stat pathway

85
Q

how do NK cells know what to kil

A

ldon’t have antigen specific receptors

have KAR receptor

86
Q

what does KAR stand for

A

KAR=Killing Activating Receptor

87
Q

if both inhibitory receptor and activating receptor are bound then NK cell wil not

A

kill cell it is interacting with

88
Q

ligand for inhibitor receptor

A

KIR

89
Q

certain viruses and tumors have properyt that they downregulate expression of

A

MHC class 1

90
Q

when viruses and stuff remove MHC class I then negative signal

A

dominantes

91
Q

receptors that transmit activating signals have in their cytoplasmic tails a sequence known as

A

ITAM

92
Q

activating receptors have

A

ITAM

93
Q

inhibiting receptors hav

A

ITIMs

94
Q

ligand for activating receptor tend to be molecules expressed on surface when cell is stressed, what family

A

MIC A

MIC B

95
Q

when cell is stressed is expresses what

A

MIC A

MIC B

96
Q

MIC A or MIC B acitvate

A

NK cells

97
Q

NK cells kill cells using same mechanism as

A

cytotoxic t cells

98
Q

how to NK cells kill

A
  1. Granule release:
    Perforins and associated molecules (form pores in target cell)
    Granzymes (proteinases that enter through pores) attack interior of target cell initiating changes leading to apoptosis
Induction of apoptosis via FasL/Fas (CD95L/CD95)
Fas ligand (FasL) on NK cell engages Fas on target cells and induces apoptosis.
99
Q

CD95 is

A

Fas

100
Q

CD95L is

A

FasL

101
Q

why is granule release more important than induction via FasL/Fas (killin by NK)

A

it’s faster

102
Q

how does granule release work

A

perforin forms pores

granzymes enter through pores and inititae apoptosis

103
Q

FasL binds to Fas to induce

A

apoptosis in cell that expresses Fas

104
Q

killer cell is cell that expresses

A

FasL

105
Q

almost every cellin body will express Fas?

A

yes

106
Q

draw out killing mechanisms for NK

A

pg 119

107
Q

bacteria and fungi what are prominent players

A

neutrophils and macrophages

108
Q

virus - what are prominent players

A

predominantly interferons and Natural Killer cells

109
Q

for paraiste what are prominent players

A

Predominantly mast cells, basophils and eosinophils

110
Q

what induces the killing of NK cells

A

IFN alpha
IFN beta
IL-12

111
Q

If there is no dominant negative signal what will NK cells do

A

kill it!