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Inflammation 4 Flashcards

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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
Dectin-1
allows fungi to be recognized and taken up - it binds to beta glucans (part of fungal cell wall)
26
macrophage has how many TLR
10 - can detect variety of pathogens
27
what is first to infiltrate infection
neutrophil
28
neutrophils are mobilized from
bone marrow
29
neutrophils once they do their job they will
die
30
the cell following neutrophil will
continue fighting or clean up dead neutrophils | monocyte → macrophage
31
cytokines that promote inflammation
IL-1, IL-6, IL-8, IL-12, Interferons, TNFs (TNF-)
32
IL12 and interferons are important in what response
innate respose against viral infections
33
once inflammatory response has done its job need what
IL-10 and TGF-β
34
IL-10 and TGF-β are
anti-inflammatory
35
IL-1, IL-6, TNF-a control
acute phase response
36
IL-1, IL-6, TNF-a iportant for promoting
acute phaseinflammation
37
interferons do qhat
Activate NK cells. | Provide anti-viral protection to neighboring cells.
38
IL is a
cytokine
39
IL-1 induces expression of
adhesion molecules on vascular endothelial cells
40
TNF alpha
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
41
Tumor Necrosis Factor-alph is
TNF alpha
42
TNF alpha important for controling
localized infection
43
systemic release of infection thats bad why
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
44
Disseminated intravascular coagulation leads to
organ failure
45
release of gram negative through body can lead to
septic shock/death
46
IL-8 signals thorugh
g proteins
47
IL-8 acitvates
integrin to allow leukocyte to pull itself into tissues
48
anti-inflammatory cytokines
IL-10 | Transforming Growth Factor- (TGF-)
49
chronic inflammation happens if
infection persists autoimune disease response to undigestible foreign material
50
hallmark of chronic inflammtion is activation of
t cells
51
activation of t cells promotes activation of
marophages
52
once t cells activated they attract more
monocytes and activate monocytes once they differente to mcrophages via cytokine IFN-gamma
53
neutrophils are secreted adn their activity associated with
TNF-alpha (secreted by T cells)
54
CD4 T cell subset aquired for cell mediated immune resposes
Th1
55
Th1 upregulate
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
Activated T cells make
IFN - gamma CD40 ligand CXCL2
57
CD40 ligand will bind to
CD40 on what cel is interacting with
58
IFN gamma and CD40 together activates
activates macrophages to destroy what they have taken up
59
CXCL2 cause
macrophages to accumulate at site of infection
60
granuloma
structure our immune system uses to wall off bacteria that we cannot eliminate - like microbacteria
61
interaction b/w th1 cells and macrophages result in formation of
granuloma
62
formation of granuloma takes
weeks to months
63
describe granuloma
fuse together and form syncitia (multinucleated giant cells) | bacteria trapped in it
64
what is doinant cell in granuloma
macrophages | tiny layer of t cells surrounding it
65
dominant effector cells in acute inflammation
neutrophils
66
dominant effector cells in chronic inflammation
Macrophages | Th1
67
innate response against viruses, who is very important in it
type I IFNs
68
type I IFN does what
primes adj cells to be much less suscpt. to promoting virus replication induce PKR and RNase L
69
Type I IFNs increase expression of
``` MHC class I enhance the ability of affected cell to show that it is infected ``` APC
70
cytotxoci t cells need what to recognize virally infected cell
MHC class I
71
APC stands for
antigen presenting cell
72
draw chart of induction of antiviral state
pg 108
73
viral genome is coactivator for
oligoadentylate synthase - this will then activate RNase L
74
during innate response of viral infection what is first thing you will see
innate cytokines being produced type I interferon IL-12
75
in vast majority of cases the innate response is not able to
eliminate infection
76
look at graph of virus titer with viral infection
pg 109
77
NK cells have ability to
kill cells infected w/ certain viruses
78
type II interferon
IFN gamma
79
production of type II interferon is restricted to which cells
NK and T cells
80
production of type I interferon by which cells
almost all cells
81
IFN gamma promotes
killing by macrophages | pdoruction of antiviral agents by uninfected cells (RNase L, etc)
82
IFN I and II increase expression of
MHC I
83
IFN II increase expression of q
MHC II
84
type II interferen signals through
jak stat pathway
85
how do NK cells know what to kil
ldon't have antigen specific receptors | have KAR receptor
86
what does KAR stand for
KAR=Killing Activating Receptor
87
if both inhibitory receptor and activating receptor are bound then NK cell wil not
kill cell it is interacting with
88
ligand for inhibitor receptor
KIR
89
certain viruses and tumors have properyt that they downregulate expression of
MHC class 1
90
when viruses and stuff remove MHC class I then negative signal
dominantes
91
receptors that transmit activating signals have in their cytoplasmic tails a sequence known as
ITAM
92
activating receptors have
ITAM
93
inhibiting receptors hav
ITIMs
94
ligand for activating receptor tend to be molecules expressed on surface when cell is stressed, what family
MIC A | MIC B
95
when cell is stressed is expresses what
MIC A | MIC B
96
MIC A or MIC B acitvate
NK cells
97
NK cells kill cells using same mechanism as
cytotoxic t cells
98
how to NK cells kill
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
CD95 is
Fas
100
CD95L is
FasL
101
why is granule release more important than induction via FasL/Fas (killin by NK)
it's faster
102
how does granule release work
perforin forms pores | granzymes enter through pores and inititae apoptosis
103
FasL binds to Fas to induce
apoptosis in cell that expresses Fas
104
killer cell is cell that expresses
FasL
105
almost every cellin body will express Fas?
yes
106
draw out killing mechanisms for NK
pg 119
107
bacteria and fungi what are prominent players
neutrophils and macrophages
108
virus - what are prominent players
predominantly interferons and Natural Killer cells
109
for paraiste what are prominent players
Predominantly mast cells, basophils and eosinophils
110
what induces the killing of NK cells
IFN alpha IFN beta IL-12
111
If there is no dominant negative signal what will NK cells do
kill it!

Immunology (12 decks)

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