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Immunology > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

1
Q

complement initiated by

A

soluble PRRs

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2
Q

during complement pathway get release of cleavage products, many components in complement pathway activated by

A

proteolytic cleavage

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3
Q

split products are

A

cleavage products that are released following activation of components of complement pathway

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4
Q

most acitivation of compeent component srequire

A

enzymatic cleavage

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5
Q

complement is important in inducing

but

A

inflammatory response

it can also cause damage to our own cells

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6
Q

don’t want complement activation on

A

surface of own cells - they can lead to lysis of own cells

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7
Q

complement consist of

A

30 plasma proteins

secreted as inactive proenzymes

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8
Q

activation of most inactive proenzymes of compleent requried

A

activation of proteolytic cleavage

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9
Q

during inflammatory response you get enhance activation of

A

complement

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10
Q

most importan function of complement in innate response

A

generate opsinin c3b
when c3b is generated covalently bind to surface ofp athogens - that acts as little flat on surface of that pathogen telling phagocyte to eat it
greaterly increases efficiency of phagocytosis

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11
Q

phagosytosis without opsinization is

A

very inefficient

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12
Q

opsinization knows what to destroy b/c

A

it has receptor for opsinin on its surface

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13
Q

when opsinin binds to bacterium the other end

A

binds to opsinin receptor on phagocyte - really high effincity -greatly enhance efficiency of phagocytosis

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14
Q

generate a lot of opsinin b/c c3 is

A

very abundant in plasma (c3 is most abundant complement component and is precurser to c3B)

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15
Q

important complement innate function

A

tell phagocyte to come in

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16
Q

c3a, c4a, c5a are

A

anaphylatoxin

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17
Q

c3a, c4a, c5a, number of affects, what are they:

A

vasculature - allows to bring more cells to area
chemoattractants - potent especially for neutrophils
stimulate mast cells

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18
Q

once c3a c4a c5a call neutrophils, what needs to happen in tissue for neutrophils to get from circulation to infected tissue

A

mast cells need to be activated

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19
Q

at end of complement cascade the complements come together in formation of a

A

pore

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20
Q

pore is called

A

mac

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21
Q

mac stands for

A

membrane attack complex

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22
Q

encapsulated bacteria, will they be sensitive to mac

A

no

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23
Q

gram + bactiera will they be sensitive to mac

will gram - be sensitive to mac

A

gram + not sensitive

gram - yes senesitive - this allows the outer part of gram neg to be taken away and the peptidoglycan part revealed

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24
Q

alternative and lectin pathway happend directly where

A

on surface of microbes or pathogens

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25
Q

classical pathway can only be activated following

A

antibody binding to antigen

usually requires adaptive response and production of antibody

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26
Q

initaters of complement activation recognize

A

PAMPs

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27
Q

3 complement pathways come together at the activation of

A

C3 (into C3a and C3b)

C3 is activated by cleavage

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28
Q

first to act, second to act, third to act of the complement activation pathways

A
  1. alternative pathway
  2. lectin
  3. classical
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29
Q

does alternative pathway require recongnition

A

no its always on

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30
Q

complement activation is the same as (another name for it)

A

complement fixation

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31
Q

what are the three pathways by which complement can become activated

A
  1. alternative pathway
  2. lectin pathway
  3. classical pathway
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32
Q

C3a and C5a recruit

C3a and C5a activate

A

phagocytes

mast cells

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33
Q

why is alternative pathway first to act

A

it is happening all the time
it’s a result of spontaneous hydrolysis of component c3 which is always happening at a low rate
it won’t go further unless there is pathogen surface

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34
Q

do lectin and classical pathway require recognition

A

yes

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35
Q

why is classical pathway the last to act

A

requires adaptive immune response

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36
Q

lectin pathway activated by

A

recognition of structures common to microbes and pathogens but not commonly found on our own cells

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37
Q

end result of the activation events

A

formation of enzyme that will cleave the most abundant component of complement: c3 - into c3a and c3b

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38
Q

c3b is the most important

A

opsinin

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39
Q

which are the chemoattractants

A

c5a
c3a
c4a

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40
Q

what initiates the alternative pathway

A

c3b binding to surface of pathogen

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41
Q

surface bound c3b now becomes binding site for plasma protein called

A

factor B

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42
Q

factor B binds to c3b and then what happens

A

factor B undergoes conformational change that makes it susceptible to cleavage by plasma protease called factor D

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43
Q

C3b is generated and covalently binds to

A

surface of pathogen

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44
Q

once C3b binds to pathogen and on its surface becomes binding site for

A

factor B

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45
Q

when factor B binds to C3b what happens

A

it undergoes conformational change that makes factor B susceptible to cleavage by plasma protease called factor D

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46
Q

some of c3b will bind to

A

enzyme that generated it and turn it from c3 converates to c5 convertase

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47
Q

properdin

A

binds to protects c3 convertase

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48
Q

absense of properdin

A

c3 convertase cleaved by factor I

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49
Q

in alternative pathway C3 convertase is

A

C3bBb

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50
Q

bacteria opsinized by

A

c3b

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51
Q

c3a diffuses and recruits

A

phagocytes

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52
Q

c3a is

A

chemoattractant

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53
Q

c3a has affects on blood vessels to allow

A

phagocytes to pull themselves through bood vessel walls and get into tissues

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54
Q

opsinization works

A

b/c phagocytes haveon surface receptor for other end of c3b, makes inefficient process very efficient

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55
Q

what is most important opsinin generated during complenet activation

A

c3b

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56
Q

what opsinin beside c3b important

A

c4b

Igg

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57
Q

Igg during adaptive response binds to

A

surface of pathogen and the other end (stem of y) binds to receptor

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58
Q

stem of Igg is called

A

Fc portion of Igg

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59
Q

receptor taht binds to stem of Igg called

A

Fc receptor

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60
Q

IgM and Igg are

A

two different types of antibodies

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61
Q

IgM is not

A

opsinin

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62
Q

IgM and Igg can also activate

A

complement pathway

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63
Q

in all pathways come c3b generated that some binds to

A

enzyme that generates it

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64
Q

when c3b binds to c3 convertase that enzyme is now

A

c5 convertase

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65
Q

c5 convertase

A

converts c5 into c5a and c5b

66
Q

c5a does what

A

goes away and attracts more phagocytes

67
Q

c5b does what

A

binds

68
Q

lectin and classical pathway have to have

A

recognition

69
Q

lectin recognition - what does it recognize

A

sugar residues by lectin

70
Q

what does lectin pathway specifically recogniae

A

mannose-binding lectin (MBL)

ficolins

71
Q

MBL stands for

A

mannose-binding lectin

72
Q

MBL and ficolin belong to

A

same family

73
Q

associated with heads of ficolin and MBL are

A

enyzmes

74
Q

once ficolin and MBl binds to something it triggers

A

conformational change which activates the first enzyme

75
Q

what are enzymes called on ficolin and MBl

A

MASPS

76
Q

how many MASPS

A

1 & 2

77
Q

MASP 1 activated by

A

conformational change

78
Q

MASP 1 does what

A

cleaves and activates MASP 2

79
Q

MASP 2 does what

A

cleaves c4 into c4 a & b

and c2 into c2a and b

80
Q

pathogens have terminal

A

mannose residues on glycose proteins

81
Q

c4a

A

goes away

82
Q

c4b

A

site of generation of c3 convertase of lectin pathway. binds to surface

83
Q

c2a

A

binds

84
Q

c2b

A

diffuses - don’t know the function

85
Q

c2a binds to

A

c4b (convertase, same as in the other pathway)

86
Q

in lectin pathway c3b functions as

A

opsinin

87
Q

classical pathway needs to be activated by

A

antibody

88
Q

antibody generated during

A

adpative resopnse

89
Q

1st component of classical pathway

A

c1

90
Q

c1 complex made of

A

c1q - c1r & c1s (two molecules of each of them associated with c1q)

91
Q

c1q binds to

A

Fc portion of antibody molecule when that antibody has bound to antigen (it will not bind to circulating antibody not bound to antigen)

92
Q

when c1q binds to Fc what happens

A

undergoes conformational change and is active

cleaves and activates c1s

93
Q

active c1r does what

A

cleaves and activates c1s

94
Q

c1 molecule has to associate with how many

A

2 molecules close together - need two fc regions close together in order to activate the classical pathway

95
Q

antibody molecule that naturally has 2 or more fc domains

A

IgM

96
Q

IgM is what kind of antibody

A

pentomer

97
Q

one molecule IgM already has

A

two Fc regions close together

98
Q

one molecule of IgM binding to C1 is

A

sufficient to activate classical pathway

99
Q

draw classical pathway

A

pg 22

100
Q

to activate classical pathway with IgG

A

need two IgG molecules bound close together

101
Q

what is most efficient antibody at activating complement

A

IgM

102
Q

one exception to classical pathway activtion

A

when molecule called CRP (c-reactive protein) binds to lipids commonly found on surface of pathogens (phosphorycholine) that allows c1q to bind directly to crp

103
Q

at the stage of C3 convertase in all three pathways will generate a lot of

A

c3b

104
Q

when c3b binds to the enzyme that generated it (c3 convertase) what does it do

A

turns c3 convertase into c5 convertase

alters the specificty of the enzyme

105
Q

c5 convertase cleaves

A

c5 - to c5a and c5b

106
Q

c5a is a potent

it also potently increases

A

chemoattractant

vascular permeabilty - causes endothelial cells to be able to be pulled apart more

107
Q

c5b is frist step in formation of what

A

first step in formation of membrane attack complex

108
Q

at what point would you begin to form the pore

A

at c5b

109
Q

MAC only perferates

A

membrane - envelope it would perforate, unencapsulated gram neg. bac. are as well

110
Q

c3a & c5a diffuse away and attract

A

leukocytes (esp neutrophils)

111
Q

c3a & c5a cause endothelial vessels lining blood vessel

A

to pull apart

enhances complement activation where infection is

112
Q

important step to allow endothelial vessels lining blood vessel to pull apart is

A

mast cells

113
Q

c3a and c5a activate what cells to de-granulate

A

mast cells

114
Q

c5b generated from c5, once generated what binds to it

A

c6

115
Q

c7 binds to

A

c6

116
Q

c7 does what

A

attaches complex to membrane

117
Q

c8 binds to

A

c7/complex

118
Q

multiple molecules of c9

A

inserts across the memberane forming pore - results in lysis of pathogen

119
Q

c8 goes

A

into the membrane

120
Q

to be lysed by membrane attack compelx MAC need to have

A

available membrane. so gram neg. more susceptible to lyssi by mac

121
Q

formation of MAC starts with

A

c5b

122
Q

what initiates mac contact with membrane

A

c7

123
Q

c8 does what

A

inserts across membrane

“c8 goes on a date - with the membrane”

124
Q

c9 does what

A

forms pores across membrane

125
Q

for c3b to funtion as opsinin ahs to be recognized by

A

receptor on phagocyte

126
Q

cr1

A

receptor for c3b & c4b

127
Q

cell that expresses cr1 has to be exposed

A

to c5a to be an opsinin

128
Q

main receptor for opsinin

A

cr1 & cr3 & cr4

129
Q

receptors on phagocytes for chemoattractats

A

c5a & c3a

130
Q

receptors on mast cells for chemoattractsns

A

c5a & c3a

131
Q

most complemet control proteins function by

A

destabilizint of convertases and ultimately degradation of convertases by factor I

132
Q

c1 inhibitor

A

removes enzymes from c1 complex and from fycolins and MBL

removes c1q and removes MBL

133
Q

can block lectin and classical pathway at start using what

A

C1 inhibitor

134
Q

just memorize the chart of regulatory proteins in classical and alternative pathways

A

pg 33

135
Q

if you destaiblize c3 convertase will never generate

A

c5 convertase

136
Q

factor I of plasma protease will

A

cleave what has been displaced

137
Q

MCP is active in which pathways

A

alternative and lectin pathways

138
Q

decay acceleration factor

A

slows acceleration of c3 convertases

139
Q

DAF stands for

what does it do

A

decay accerlerating factor - accelerates decay of convertases

140
Q

CD59

A

prevents insertion of c9 across the membrane

prevents formation of pore membrane attack complex

141
Q

C1 inhibitor removes enzymes from

A

initiatiors of classical and lectin pathway

142
Q

defficient levels or defective C1 inhibitor is what disease

A

Hereditary Angioedema - HAE

143
Q

C1 inhibitor prevents production of what part of acute inflammation

A

bradykinin

144
Q

bradyknin is

A

potent inducer of vascular permeability

145
Q

disregulated production of bradykniin leads to

A

increase in vascular permeability at the point of trauma - so movement of fluid into the tissue leading to swelling (hereditary angioedema)

146
Q

iC3b fragments can function as

A

opsinin - but do not have active convertase. only incative in terms of convertase activity

147
Q

DAF, MCP, C4BP, CR1

A

dirsupt c3 convertase formation

148
Q

c3 convertase necessary to generate

A

c5 convertase - will nver form the pore

149
Q

c5 convertase required for genreation of

A

c5b

150
Q

CD59 binds to

A

c5b678

151
Q

cd59 prevents

A

echo 11:10

152
Q

no functional cd59 is what disease?

A

Paroxysmal Nocturnal Hemoglobinuria - PNH

153
Q

most sensitive cells to complement mediated lysis

A

RBC

154
Q

PNH stands for

A

Paroxysmal Nocturnal Hemoglobinuria

155
Q

result in de novo mutations in gene that is required to anquor the complemetnt regulatory proteins to the cell memvrane

A

PNH

156
Q

when factor D cleaves factor B it splits off what fragment

what remains bound to C3b

A

Ba

Bb remains bound to C3b

157
Q

C3b functions as an

A

opsinin

158
Q

What is the CD name for DAF

A

CD55

159
Q

What is the CD name for MCP

A

CD46

160
Q

write out the diagram (or understand)

A

pg 42

161
Q

write out the diagram (or understand)

A

pg 43

162
Q

understand the diagram

A

pg 44

Immunology (12 decks)

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