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immuno exam 2 Flashcards

1
Q

3 pathways of complement activation

A

lectin
classical
alternative

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2
Q

complements are activated mostly through

A

alternative pathway

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3
Q

major components of lectin pathway

A

MBL
ficolins
MASP-2
C2-C9

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4
Q

how is lectin pathway activated

A

when mannose binding lectin (MBL) or ficolin binds to pathogen surface

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5
Q

part of the lectin pathway, MASP-2 cleaves

A

C4 into C4a and C4b
C2 into C2a and C2b

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6
Q

part of lectin pathway, C4b bound to C2b (C4bC2b) generates

A

C3 convertase

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7
Q

part of lectin pathway, C3 convertase cleaves

A

C3 into C3a and C3b

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8
Q

part of lectin pathway, C3b binds to C4bC2b (C4bC2bC3b) to generate

A

C5 convertase

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9
Q

part of the lectin pathway, there are many ___ molecules on the pathogen surface
C3 convertase can cleave up to 1000 of this molecule

A

C3b

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10
Q

major components of classical pathway

A

C1q
C1r
C1s
C2-C9

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11
Q

the first component activated in the classical pathway

A

C1

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12
Q

C1 is activated by

A

antibody-antigen complexes

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13
Q

part of the classical pathway, 3 subunits of C1

A

C1q
C1r
C1s

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14
Q

part of the classical pathway, which molecule is converted into an active protease

A

C1s

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15
Q

which Ab is most efficient at activating the classical pathway

A

IgM

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16
Q

part of the classical pathway, active C1s cleaves C4 into

A

C4a and C4b

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17
Q

part of the classical pathway, __ binds to C4b, generating C4b2

A

C2

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18
Q

part of the classical pathway, C1s cleaves C42b into

A

C2a and C4b2b

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19
Q

part of the classical pathway, C4b2b is also called

A

C3 convertase

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20
Q

part of the classical pathway, C3 convertase cleaves C3, generating

A

C4b2b3b (C5 convertase)

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21
Q

major components of alternative pathway

A

C3
B
D
P
H
I
C5-C9

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22
Q

how is the alternative pathway activated

A

membrane bound C3b generated from lectin/classical pathway; spontaneous hydrolysis of C3

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23
Q

part of alternative pathway, B factor binds to C3b on the pathogen surface; B factor is then cleaved by ___ into Ba and Bb, generating C3bBb

A

factor D

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24
Q

part of alternative pathway, C3bBb is

A

C3 convertase

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25
Q

why does C3b need to be destroyed as fast as it gets generated

A

to prevent over-activation of the complement

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26
Q

part of alternative activation, what molecules bind to C3b on the host cell surface to prevent C3b from binding to other molecules and activating the complement

A

DAF
I
H
MCP
CR1

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27
Q

part of alternative pathway, what molecule stabilizes C3 convertase on the pathogen surface; makes sure the complement can be activated

A

properdin (factor P)

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28
Q

part of alternative pathway, C3b binds to C3bBb to generate

A

C3bBbC3b (C5 convertase)

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29
Q

the last component to be cleaved by the complement

A

C5

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30
Q

first step of forming membrane attack complex (MAC)

A

activating C5

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31
Q

C5 convertase from all 3 complement pathways bind and cleave

A

C5 into C5a and C5b

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32
Q

to form MAC, C5b binds to

A

C6 and C7
generating C5b67 complex

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33
Q

to form MAC, C5b67 binds to pathogen membrane via

A

C7

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34
Q

to form MAC, C8 binds to C5b67 complex and inserts into

A

pathogen cell membrane

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35
Q

to form MAC, C9 binds to C5b678 complex and polymerizes into 10-16 molecules of C9, forming a pore in the pathogen’s cell membrane, this is destructive because

A

it allows water to get into and destroy the cell

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36
Q

for complement regulation, what molecule is a C1 inhibitor; binds to C1s

A

C1NH

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37
Q

for complement regulation, what molecules inactivate C3 convertase; displace C2b from C4b2b

A

DAF
CR1
MCP
C4BP

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38
Q

for complement regulation, what molecules inactivate C5 convertase; binds to C3b

A

CR1
H factor
I factor

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39
Q

for complement regulation, which factor cleaves C3b

A

I factor

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40
Q

for MAC regulation, what molecule blocks the formation of MAC; binds to C5b678 to prevent C9 binding

A

CD59 (Protectin)

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41
Q

3 consequences of complement activation

A

direct killing of pathogens
promote phagocytosis of pathogens
promote inflammation

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42
Q

which complement molecule serves as an opsonin to promote phagocytosis

A

C3b

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43
Q

which complement molecule is necessary to stimulate phagocytosis

A

C5a

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44
Q

how do C3a and C5a promote inflammation

A

binding to cel surface increases vascular permeability and infiltration of inflammatory cells in tissues

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45
Q

complement gene clusters of ___ in MHC III region

A

C4, C2, factor B

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46
Q

complement gene clusters of ___ in RCA cluster

A

C4BP, CD55, CD35, CD21, CD46, factor H

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47
Q

pattern of genetic variants in complement genes inherited by an individual

A

complotype

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48
Q

C4-4 allele expression is associated with

A

low serum C4
autoimmune polyarthritis development in dogs

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49
Q

autosomal hereditary recessive C3 deficiency is caused by

A

deletion of single cytosine
frameshift mutation - pre mature stop codon
shortened C3 chain

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50
Q

clinical effect of autosomal hereditary recessive deficiency

A

seen in brittany spaniels
heterozygous - normal
homozygous - inc susceptibility to bacterial infections

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51
Q

porcine factor H deficiency is

A

autosomal recessive in yorkshire pigs

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52
Q

clinical effect of porcine factor H deficiency

A

healthy at birth
failure to thrive
stop growing
become anemic
die of renal failure due to excess C3b

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53
Q

treatment of porcine factor H deficiency

A

replace factor H by plasma transfusion

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54
Q

tests for porcine factor H deficiency

A

electron microscope
indirect immunofluorescence

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55
Q

effect of mannose binding lectin deficiency

A

inc susceptibility to infections in children
not yet described in domestic animals

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56
Q

effect of C6 or C7 deficiency

A

individuals are healthy

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57
Q

what do MHC deliver

A

pathogen signals to T cells

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58
Q

what were MHC originally discovered as

A

transplantation antigens

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59
Q

what do MHC play a role in recognizing

A

intercellular recognition and self vs. non-self

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60
Q

what do T cell receptors (TCR) recognize

A

an Ag derived peptide combined with MHC on an APC

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61
Q

how many classes of MHC molecules are there

A

3

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62
Q

what forms the antigen binding site on MHC I; area the T cell sees

A

a1 and a2 chain

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63
Q

how large are antigenic peptides MHC I binds

A

8-10 amino acids

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64
Q

what forms the floor of MHC 1

A

B pleated sheet

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65
Q

what forms the walls of MHC 1

A

two parallel alpha helices

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66
Q

a3 domain on MHC 1 has a binding site for

A

CD8 molecules for phagocytosis

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67
Q

how many chains does MHC II contain

A

2, a and B

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68
Q

what region of MHC II does a T cell antigen receptor see

A

a1, B1 and antigenic peptide

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69
Q

how large is the antigenic peptide on MHC II

A

13-25 amino acids

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70
Q

the antigen binding site on MHC II is formed by

A

a1 and B1 domains

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71
Q

on MHC II, a2 and B2 domains have a binding site for

A

CD4 molecules

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72
Q

how do MHC molecules bind to peptides

A

anchor residues; can bind many different peptides

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73
Q

MHC III

A

do not directly participate in antigen processing and presentation

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74
Q

what properties of MHC molecules make it difficult for pathogens to evade the immune response

A

polygenic and polymorphic

75
Q

what makes MHC polygenic

A

MHC molecules have two major different classes, each with different loci

76
Q

what makes MHC polymorphic

A

each MHC locus has two alleles in an individual; creates genetic diversity and prevents a pathogen from eliminating an entire species

77
Q

what kind of MHC molecules have similar structure but are less polymorphic in a population

A

nonclassical MHC I

78
Q

what 2 mechanisms contribute to MHC polymorphism

A

point mutations
gene conversion

79
Q

gene conversion

A

small blocks of DNA are exchanged between different class I genes in a nonreciprocal fashion

80
Q

the more diverse MHC molecules an individual has

A

the higher chance of presenting self-antigens and autoimmune disease, and the smaller the peripheral T cell repertoire

81
Q

ideal number of MHC molecules in humans for maximizing foreign Ag recognition and minimizing self Ag recognition

82
Q

presence of HLA alleles DR4 and DRQ are associated with more susceptibility to

A

type 1 diabetes

83
Q

presence of HLA alleles B57 and B27 are associated with

A

more susceptibility to psoriasis, ankylosing spondylitis and reiter’s syndrome
overrepresented in the HIV elite controllers (undetectable HIV)

84
Q

presence of BoLA-DRB3.2 7, 8, 11, 22, 24 and 28 alleles is associated with

A

low proviral load for bovine leukemia virus

85
Q

presence of BoLA-DRB3.2 10 allele is associated with

A

high proviral load for bovine leukemia virus

86
Q

antigen

A

substance capable of stimulating immune response; activates lymphocytes

87
Q

epitope (antigenic determinant)

A

portion of Ag that binds to immune cells

88
Q

where do B cell epitopes present

A

surface of molecule

89
Q

a large molecule with multiple epitopes can

A

stimulate multiple immune responses

90
Q

what part of epitopes do B cells recognize

A

conformation of epitope

91
Q

T cell epitopes come from

A

large molecules like bacteria; can be located anywhere in molecule

92
Q

how do T cells recognize epitopes

A

if bound to APC on MHC

93
Q

Ag that invade a host from outside and then grow in the host’s tissues and extracellular fluid; processed in phagosomes in APCs; typically bacterial

A

exogenous Ag

94
Q

Ag produced by host cells; processed by proteasomes in the cells they are produced; viral or autoantigens

A

endogenous Ag

95
Q

two properties of Ag

A

immunogenicity
antigenicity

96
Q

ability of an Ag to provoke an immune response in the body

A

immunogenicity

97
Q

capacity of an Ag to bind specific T cells or B cells

A

antigenicity

98
Q

factors that determine the immunogenicity of an Ag

A

foreignness
size
stableness
complexity
genetics of recipients
route of Ag administration
dose of Ag

99
Q

has antigenicity but not immunogenicity; only immunogenic when bound to other large molecules; activates immune response when attached to a carrier

100
Q

what cells can serve as APCs

A

nucleated cells that express MHC

101
Q

what cells cannot serve as APCs

102
Q

MHC class II only present on

A

professional APCs

103
Q

professional APCs

A

dendritic cells
macrophages
B cells

104
Q

what is the only APC that can activate naive T cells

A

dendritic cells

105
Q

DCs are not found in

A

immune privileged sites
brain, eyes, testes

106
Q

where are DCs prominent

A

lymph nodes
skin
mucosal surfaces

107
Q

purpose of dendrites on DCs

A

inc surface area - inc efficiency of Ag trapping and maximize contact between DCs and other cells

108
Q

DC type specialized in taking up, processing and presenting Ag to naive T cells

A

classical or conventional DCs (cDCs)

109
Q

DC type that responds to viruses by synthesizing type 1 IFN; also synthesizes type 3 IFN; can activate NK cells

A

plasmacytoid DCs

110
Q

DC type in the skin

A

langerhans cells

111
Q

DC type found in the germinal centers of spleen, LN and peyer’s patches; found in localized infection sites; essential for Ab production and B cell memory

A

follicular DCs

112
Q

role of immature DCs

A

capture invading microbes; capture Ags by phagocytosis, pinocytosis and by binding to cell surface receptors; does not completely degrade pathogens

113
Q

how do immature DCs kill invaders

A

mounting respiratory burst

114
Q

role of activated DCs

A

present Ags to T cells
activate T cells

115
Q

what do activated DCs respond to

A

IL-1
TNF-a
PAMPs and DAMPs

116
Q

mature DCs express DC-SIGN that binds ICAM-3, what is the function of this interaction

A

allows DCs to maintain a prolonged interaction with naive T cells and rapidly screen 1000s of T cells

117
Q

why are macrophages inefficient APCs

A

most of ingested Ag is destroyed by lysosomal proteases and oxidants

118
Q

B cell antigen receptors (BCRs) enable B cells to

A

present large amounts of specific Ags to sensitized T cells

119
Q

4 important molecules for MHC II

A

invariant chain - CLIP
HLA-DM
HLA-DO
MARCH-1

120
Q

CLIP is part of an invariant chain for MHC II, what is its function

A

binds to MHC II to stabilize before peptides are available

121
Q

function of HLA-DM

A

catalyzes the release of CLIP and binding of antigenic peptides to MHC II

122
Q

function of HLA-DO

A

negative regulator of HLA-DM; binds to DM to prevent peptide loading of MHC II

123
Q

function of MARCH-1 (membrane bound E3 ligase)

A

regulates MHC II Ag processing and presentation

124
Q

important molecules for MHC I Ag processing and presentation

A

TAP
ERAAP
proteasome

125
Q

function of TAP

A

transporting peptides generated from proteasome into ER

126
Q

TAP expression is enhanced by

A

interferon

127
Q

function of ERAAP

A

trim amino termini of peptides before binding to MHC I molecules

128
Q

ERAAP expression is enhanced by

129
Q

function of proteasome

A

process Ag under physiological conditions

130
Q

PA28 proteasome-activator complex is induced by

131
Q

exogenous Ag can be loaded on to MHC I molecules via

A

cross presentation

132
Q

endogenous Ag are loaded on to MHC II molecules via

A

autophagy pathway

133
Q

4 cytokine families

A

interleukin
interferon
TNF
chemokines

134
Q

cytokine modes of action

A

autocrine/intracrine
paracrine
endocrine

135
Q

properties of cytokines allow

A

cytokines to regulate the activity of immunocompetent cells in a coordinated manner

136
Q

cytokine property: a given cytokine has different biological effects on target cells

A

pleiotropic action

137
Q

cytokine property: two or more cytokines exert the same biological effect on the same cells

A

redundancy

138
Q

cytokine property: effect of two cytokines on a particular cell is greater than the additive effect of individual cytokines

A

synergistic action

139
Q

cytokine property: the action of one cytokine inhibits the effects of another cytokine

A

antagonistic action

140
Q

ex of two synergistic cytokines

A

IL-4 and IL-5
stimulate B cell proliferation and induces class switch to IgE

141
Q

ex of two antagonistic cytokines

A

IL-4 and IFN-y
IFN-y blocks class switch to IgE induced by IL-4

142
Q

cytokine property: action of a cytokine leads to the induction of one or more cytokines which in turn induces the production of other cytokines

A

cascade action

143
Q

cytokines have at least two functional units on their cell surface receptors; what are they for

A

ligand binding
signal transduction

144
Q

what type of receptor is not used as a cytokine receptor

A

channel linked receptor

145
Q

receptors that use tyrosine kinases for intracellular signaling are typical for

A

growth factor and cytokine receptors

146
Q

immunological receptors that use GPCR

A

C5a
chemokine receptors
leukotriene receptors
platelet activating factor receptor

147
Q

ligation of sphingomyelinase activating receptors triggers

A

activation of NF-kB

148
Q

sphingomyelinase activating receptors are often used by

A

IL-1 and TLRs

149
Q

group 1 cytokine receptors form complexes with

A

janus kinases (JAKs)

150
Q

what do JAKs do

A

phosphorylate STAT

151
Q

what does STAT do

A

dimerizes to form an active transcription factor; may enhance or suppress cytokine signaling

152
Q

central to most cell signaling; reversible modification of proteins by adding a phosphate group to selected amino acids

A

protein phosphorylation

153
Q

signal transduction systems use __ to modify and send a signal into a cell

154
Q

amino acids phosphorylated by protein kinases

A

serine
threonine
tyrosine

155
Q

phosphorylation of this amino acid is key in cytokine receptor signal transduction

156
Q

three major signal transduction pathways in the immune system

A

NF-kB pathway
NF-AT pathway
JAK-STAT pathway

157
Q

highest distribution of lymphocytes in

A

lymph nodes

158
Q

discovery of T cells by

A

thymectomy; loss of cellular immunity

159
Q

discovery of B cells by

A

bursectomy; loss of humoral immunity

160
Q

what technique can be used to identify molecules expressed by lymphocytes

A

fluorescence activated cell sorting (FACS) using a flow cytometer

161
Q

types of lymphocyte surface molecules

A

adhesion molecules
Ag receptor complex
molecules that regulate lymphocyte function

162
Q

how do lymphocytes use adhesion molecules

A

naive LC use to migrate into lymph nodes
LC use to migrate into inflamed tissues and to interact with other cells

163
Q

ex of adhesion molecules

A

ICAM-1
VCAM-1
interact with LFA-1

164
Q

chains on T cell Ag receptor complex (TCR)

A

alpha-beta chain
gamma-delta chain

165
Q

what molecule transmits TCR signal into a cell

166
Q

what molecule is the coreceptor on CD4+ T cells and necessary for Ag recognition for MHC II

167
Q

what molecule is the coreceptor on CD8+ T cells and necessary for Ag recognition for MHC I

168
Q

B cell Ag receptor (BCR) is

A

membrane bound Ab;
can loosely bind then change to have high affinity

169
Q

what molecules transmit BCR signal into a cell

A

Iga (CD79a)
IgB (CD79b)

170
Q

2 important B cell co-receptor molecules

A

CD19 and CD21

171
Q

what molecule is a co-stimulatory receptor and necessary for naive T cell activation

172
Q

what receptor is an important growth factor for activated T cells

A

IL-2 receptor

173
Q

what molecule is a marker for an active T cell; naive T cells do not express

174
Q

lymphocyte surface molecules expressed on naive T cells

A

CD45RA
CD127

175
Q

lymphocyte surface molecules expressed on effector T cells

A

CD25
CD45RA/RO (not highly expressed)

176
Q

lymphocyte surface molecules expressed on effector memory T cells

A

CD45RO
CD127

177
Q

lymphocyte surface molecules expressed on central memory T cells

A

CD25
CD45RO
C127

178
Q

lymphocyte mitogens

A

activate lymphocytes in a non-Ag specific way; used to measure lymphocyte functions

179
Q

commonly used mitogens

A

PHA
Con A
PWM
LPS

180
Q

which mitogen:
from red kidney bean
binds N-acetylgalactosamine
stimulates T cells, a little bit B cells

181
Q

which mitogen:
from jack bean
binds a-mannose and a-glucose
stimulates T cells

182
Q

which mitogen:
from pokeweek plant
both T and B cells

183
Q

which mitogen:
from gram negative bacteria
stimulates B cells

immunology (2 decks)

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