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Immunology Block 4 > Review > Flashcards

Review Flashcards

1
Q

cell wall in gram pos

A

peptidglycan layer outside cell membrane

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2
Q

what add’l feature present in gram pos and neg

A

capsule

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3
Q

what does capsule do

A

makes bacteria difficult to phagocytes to deal with unless it can be opsonized

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4
Q

compare and contrast gram neg and gram pos bac

A

ppt

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5
Q

what Ig do we need to opsinize capsule

A

IgG

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6
Q

difference b/w cell wall of gram pos and gram neg

A

thickness

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7
Q

what do we use to do use to differentiate if its gram pos or gram neg

A

gram stain

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8
Q

gram pos vs gram neg cell wall

A

gram pos 10x thicker

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9
Q

gram stain does what with gram pos

A

it’s trapped - crystal violet die is trapped so stained purple “violet”

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10
Q

gram pos will stain

A

blue (purple)

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11
Q

gram pos associated with the cell wall

A

teichoic acid & lipoteichoic acid

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12
Q

what two things are unique to gram pos

A

teichoic acid

lipoteichoic acid

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13
Q

describe gram stain and list the steps

A 
to see if bacteria is pos or neg.
fixation
crystal violet
iodine treatment
decolorization
counter stain safranin
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14
Q

LPS is part of gram pos or neg

A

gram neg

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15
Q

what TLR to detect LPS

A

TLR4

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16
Q

what is the toxic component of LPS

A

Lipid A component

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17
Q

four main mechanisms stuff can be transffered b/w bac

A

transposition
transformation
conjugation
transduction

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18
Q

transposition

A

transposons

the movement of small pieces of DNA called transposons to different locations in the genome and between plasmids. These are sometimes called “jumping genes.”

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19
Q

transformation

A

ability of bacterium to take up DNA from enviornment and stabilize by recombination into own chrom

“uptake of naked DNA”

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20
Q

conjugation

A

transfer of plasma DNA following contact or transfer of bacterial chromosomal genes if it recombines, then can transfer bacterial chromosomal genes that lie closest to the insertion point of the plasmid

the transfer of DNA through cell-to-cell contact

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21
Q

transduction

A

exchange of genetic info mediated by viruses that infect bac

the transfer of genetic information via bacterial viruses (phages).

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22
Q

two main mechanisms of transduction

A

generalized

specialized

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23
Q

generalized transduction what cycle

A

lytic cycle

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24
Q

specialized transdicution mediated by

A

lysogenic or temperate phages

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25
Q

lysogenic phages do what

A

integrate their DNA into DNA of bacerial cell and can remain there for life of bacteria as prophage

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26
Q

during latent stage describe phage DNA

A

not silent

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27
Q

if bacterium becomes friend prophage can be

A

reactivated

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28
Q

mistsake that leads to specialized transduction

A

sometimes it doesn’t come out exactly the right way - sometimes it can be half infectious half not.

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29
Q

review pg 6 and understand - review ppts if don’t understand

A

pg 6

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30
Q

F+ by F- cross what are you doing

A

transferring conjugal plasmid

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31
Q

male cell has

A

f pillus

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32
Q

single strand cleaveage at

A

origin of transfer

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33
Q

conjugation and transfer you need

A

male and female

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34
Q

at the end of conjugateion both cells

A

are donor cells

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35
Q

all that is transferred in conjugation transfer are

A

genes on plasmid

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36
Q

main difference b/w F+ F- and Hfr

A

all that is transffered on F+ F- is plasmid

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37
Q

Hfr cross where does it always happen

A

origin of tranfer

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38
Q

Hfr cross you will never transfer

A

genes encoding F pillus

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39
Q

why won’t you ttansfer genes for f pillus at Hfr cross

A

they are the very end and they don’t get transffered

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40
Q

to be able to transfer the f pillus you have to transfer what for Hfr

A

entire DNA for Hfr

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41
Q

what is end result of Hfr

A

recipient always F-

it may aquire bacterial chromosomal genes from donor

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42
Q

what does a virus need to have

A

genome

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43
Q

what kind of genome can virus have

A

DNA or RNA

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44
Q

DNA genomes in virus can be

A

linear or circular

single-stranded or double stranded

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45
Q

RNA genome can be

A

linear or segmented

single stranded or double stranded

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46
Q

infleunza is example of virus with

A

segmented genome

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47
Q

positive sense RNA is

A

like mRNA

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48
Q

negative sense RNA pripor to translation

A

have to be converted to positive sense

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49
Q

positive sense RNA prior to translation

A

cn just be translated, its like mRNA

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50
Q

ambisense means

A

+ at one end - at the other end

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51
Q

positive sense RNA viruses do not need

A

RNA dep RNA pol

but they encode it

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52
Q

two structures possible for capsid

A

helical or icosahedral

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53
Q

all that naked virus is

A

capsid genome

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54
Q

enveloped viruses have what on outiside

A

lipid bilayer - from host cell when they budded

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55
Q

how do virus get envlope

A

from budding from host cell

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56
Q

what is envelope for virus

A

lipid bilayer

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57
Q

what are the targets for neutralizing antiodies for viruses

A

peplomers

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58
Q

if virus needs something host cell cannot provide then

A

virus has to bring it with it

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59
Q

examples of packaged enzymes for virus

A

replicases

proteases

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60
Q

structural proteins

A

part of the virion itself

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61
Q

non-structural proteins

A

not part of virion

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62
Q

virally encoded enzymes are not always packaged in

A

virion

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63
Q

if something is required to get to mRNA then they have to be what in virus

A

packaged

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64
Q

if somethign is needed after mRNA stage for virus replication they have to be what in virus

A

encoded doesn’t need to be packaged

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65
Q

naked virus is released by

A

lysis

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66
Q

enveloped virus are released by

A

budding

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67
Q

what steps do all viruses need to go through intheir life cycle

A 
adherence
penetration
replication
assembly
release
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68
Q

HIV fuses at what pH

A

neutral

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69
Q

influenza virus fuses at what pH

A

acidic

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70
Q

what is pH independent fusion

A

neutral pH fusion

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71
Q

what is pH dependent fusion

A

acidic pH fusion

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72
Q

b/c influenza virus will only form at acidic pH cannot form

A

syncytia

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73
Q

HIV and other things that fuse at neutral pH can form

A

syncytia

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74
Q

review replication strategies of virsues

A

pg 13

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75
Q

site of replication dictates what dna virus

A

has to bring with it

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76
Q

vast majority of dna viruses replicate in

A

nucleus

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77
Q

vast majority of rna viruses replicate in

A

cytoplasm

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78
Q

rna virus replication exception

A

orthomyxoviruses replicate in nucleus

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79
Q

dna virus replication exception

A

poxviruses replicate in cytoplasm

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80
Q

depending on the cell that dna virus replicates is a replicating cell or quiescent determiens

A

if they need to bring polymerase with them

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81
Q

quiescent cells don’t have what

A

polymerase b/c they won’t be replicating

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82
Q

retroviruses and hepadnaviruses replicate where

A

both - have stage in cytoplasm and nucleus

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83
Q

can get formation of what for viruses that replicate in nucleus

A

intranuclear inclusion bodies

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84
Q

if enzyme is required for production of mRNA and cell cannot provide it must be

A

pakcaged

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85
Q

if enzyme is not needed to get to mRNA but is required in replication and host cell cannot provide it must be

A

encoded, but doesn’t need to be packaged

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86
Q

chitin rechognized by

A

TLR2

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87
Q

LPS recongized by

A

TLR4

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88
Q

flagellin recognized by

A

TLR5

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89
Q

beta-glucan recognized by

A

dectin-1

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90
Q

viral nucleic acid intracellular PRR

A

TLR3, 7, RIG-I

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91
Q

bacterial DNA intracellular PRR

A

TLR9

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92
Q

pRR is a

A

pattern recogniztion receptor

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93
Q

lipids etc of intracellular bacteria PRR

A

NOD1 NOD2

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94
Q

mannosylated molecules can be recongized by

A

MBL & Ficolins & lectin

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95
Q

antibody bound to pathogen can be recognized by

A

C1q

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96
Q

need how many IgG for C1q to bridge gap

A

2 - only need 1 for IgM

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97
Q

when c reactive protein binds to lipid on surface of bacteria it allows

A

c1q to bind directly to reactive protein

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98
Q

review the complement video

A

:)

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99
Q

for direct activation of pathogen surface is what pathway

A

alternative

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100
Q

just reivew my compleemtn chart and the video

A

.

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101
Q

low levels of C2 and C4 predispose you to?

A

immune complex disease

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102
Q

defect in C1-INH what disease

A

HAE

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103
Q

CD45 is

A

DAF

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104
Q

DAF stands for

A

decay accelerating factor

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105
Q

C3b is

A

opxinin

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106
Q

C3b allow

A

phagocytes to bind and enhances the ability of phagocyte to take up bacterium and destroy

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107
Q

what is the highest concentration in complement

A

C3

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108
Q

C5a is

A

chemoattractant

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109
Q

C3a is

A

chemoattractant

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110
Q

C3a and C5a are chemoattractant and they also attract

A

mast cells

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111
Q

what is first part of mac formation

A

C5b

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112
Q

an anything prevent formation of MAC on our own cells?

A

CD59

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113
Q

CD59 is also known as

A

protectin

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114
Q

protectin does what

A

stops complement from forming on our own cells

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115
Q

low levles of C3 susceptible to

A

recurrent bactieral infections, esp with encapsulated bacteria

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116
Q

no MAC, suscpetible to

A

nisseria infections

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117
Q

when is complement activated

A

following binding of initiators to pathogen surfaces

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118
Q

C1q is part of which complement ptahway

A

classical

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119
Q

MBL/ficolins pat of which compelemtn apthway

A

lectin

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120
Q

C3b is part of what complement pathway

A

alternative

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121
Q

MAC causes lysis of what two things

A

gram neg

enveloped

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122
Q

what attacks gram pos bacteria

A

lysozyme

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123
Q

c3b and c4b are

A

opsinins

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124
Q

c5 and c3 a are

A

leukocyte chemoattractants

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125
Q

c5a and c3a increase

A

vascular premeability, complement proteins, and bradykinin

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126
Q

bradykinin mediates

A

pain

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127
Q

c5a and c3a induce

A

mast cell activation and degranulation

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128
Q

binding of PAMp to mast cell PRR can induce

A

degranulation

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129
Q

mediators relased by mast cells

A

histamine
TNF alpha
IL-1
IL-8

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130
Q

what does TNF alpha and IL-1 do

A

increase vascular permeability

increase adheion molecules on vascular endothelial cells (allows phagocytes to bring themselves to a halt)

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131
Q

most potent chemoattractant for neutrophils

A

IL–8

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132
Q

IL-8 is

A

leukocyrte chemoattractant

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133
Q

IL-12 activates

A

NK cells

and signal 3 for differentation of CD4 into Th1 cells

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134
Q

TNF alpha, IL-1, and IL-6 induce

A

acute phase response

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135
Q

what is always first cell at site of inflammation

A

neutrophils

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136
Q

what is most abundant leukocyte

A

neutrophils (also the fastest!)

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137
Q

draw out leukocyte extravasation from tissues

A

pg 23

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138
Q

dissease cD18 is defective

A

LAD1

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139
Q

disease CD 15 defective?

A

LAD II

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140
Q

draw out steps of phagocytosis

A

pg 24

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141
Q

gram neg bac will stain

A

pink

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142
Q

LPS (lipopolysacchardie) is also called

A

endotoxin

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143
Q

besides TLR4 what detects presence of LPS

A

LPS binding protein & CD14

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144
Q

main killing mechanism of neutrophils

A

oxidative killing

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145
Q

oxidative killing mechanism dependent on what complex

A

NADH oxidase

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146
Q

oxidative pathway of killing is induced by

A

exposure to chemoattractants

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147
Q

besides oxidative killing pathway what can neutrophils do

A

non-oxidative killing

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148
Q

what are examples of enzymes in non-oxidative killing pathway

A

elastase
cathespins/orher proteinases
colalgenase
lactoferrin

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149
Q

lack of oxidative pathway is not sufficient, how do we know

A

chronic granulomas disease

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150
Q

during inflammation greatly increase prduction of ____ from bone marrow

A

neutrophils

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151
Q

after neutrophil what is next cell to enter site of infection

A

monocyte

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152
Q

most of neutrophils that fight site of infection will

A

die :(

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153
Q

macrophaegs come in after neutrophils to

A

clean up the pathogen and the dead and dying netrophils

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154
Q

what is netosis

A

explosive death of netruphils where they expell their proteins

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155
Q

what does netosis expell

A

histones, degradative enzymes, proteinase 3, especially PEPTIDYL ARGININ DEIMINIASE (PAD)

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156
Q

NETs stands for

A

neutrophil exraclular Traps

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157
Q

nets function as

A

traps for bacteria - make the bacteria more easily to deal with by monocytes (macrophages)

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158
Q

when monocytes arrive at site of infection they differentiate into

A

macrophaegs

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159
Q

notecard pg 29

A

29

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160
Q

when dendritic cells acquire antigen and they are migrating to lymph node they are

A

processing antigen so they are ready to present antigen to t cell when they get to lymph

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161
Q

explain exogenous pathway

A

pg 31

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162
Q

expalin endogenous pathway

A

pg 31

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163
Q

endogenous pathway

A

processing antigen made inside cell

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164
Q

exogenous pathway

A

processing antigen take up from outside cell

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165
Q

acidic vesicles are responsibel for

A

processing of antigen into peptides

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166
Q

endosome becomes progressivly

A

acidified

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167
Q

drop in PH activates

A

the things that will degrade antigens into short peptides

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168
Q

which MHC for exogenous pathway

A

MHC class II

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169
Q

what is antibody good at

A

good at getting what is outside of cells

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170
Q

restrict activation of CD4 t cells to peptides derviced from amterial that comes in from

A

outside of cell -b /c it will help b cells make antibody against the material

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171
Q

t cell epitope and b cell epitopes have to be

A

linked

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172
Q

to help b cell make antibody against extraclelular antigen

A

must be linked to t cell

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173
Q

invariant chain describe function

A 
block class II from binding peptides from endogenous material
binds to MHC II, blocks binding groove and stops things that shoudl bind to MHC I to bind to MHC II

redirects class II to where the peptides are - endosomal comparemtnt

174
Q

what is CLIP

A

what is left in MHC II binding groove after it has been cleaved

175
Q

HLC-DM catalyzes change of

A

CLIP for peptide

176
Q

immunoproteasome

A

cleaves proteins into short peptides

177
Q

in ER peptides that are gnerated bby proteasome can bind to MHC I then

A

disassociates from calenxin and geos to calreticulin

178
Q

what does calnexin do

A

holds MHC I until beta2M arrives

179
Q

draw out endogenous pathway

A

check iwth old notes to get right

180
Q

draw outexogenous pathway

A

check with old notes to get it right pg 31

181
Q

eptiopes for b cells tend to be

A

hydrophilic

182
Q

peptides recognized by t cells tend to be

A

hydrophobic

183
Q

MHC required for b cells

A

no

184
Q

mhc required for t cells

A

yes

185
Q

10:44

A

put in the proper slide it’s weird in my power point

t cell and be cells arise from common progenitor cell

186
Q

draw out/explain the maturation of t cell and b cell

A

pg 33

187
Q

heavy chain locus made up of

A

VDJ

188
Q

always which locus to rearrange first

A

heavy chain

189
Q

after heavy chain has passed test for functionality (tested by surgoate light chain ) then you will

A

rearrange kappa or lambda light chain (humans use kappa more)

190
Q

process that heavy chain and light chain brought otgether

A

somatic recombination

191
Q

first locus to rearrange always

A

heavy chain

192
Q

light chain rearrangement governed by what rule

A

12 23 rule

193
Q

following rearrangement for light chain you bring what together

A

VJ

194
Q

first rearrangement in heavy chain

A

DJ

195
Q

second rearrangment in heavy chain

A

DJ then VDJ

196
Q

after chain rearrangment, list steps

A 
transcription
primary RNA trancript
RNA pslicing
mRNA
translation
H or L protein
197
Q

what are enzymes responsible for rearrangment of chains

A

RAG1
RAG2
Tdt
artemis (omenn)

198
Q

assumign we arrange functional beta chain we are almost certain to

A

rearrange functional alpha chain

199
Q

how many chances to rearrange alpha chain

A

lots

200
Q

first rearrangment of beta chain lcous

A

DJ then VDJ

201
Q

rearrangment at alpha chain locus

A

VJ

202
Q

CDR3 not encoded in

A

germline - it’s generated in recombination process

203
Q

CDR3 is most variable b/c

A

imprecision involved in joining

204
Q

n nucleotide addition by

A

TdT

205
Q

first rearragnemtn in b cell

A

D to J in heavy chain

206
Q

first rearrangment for t cell

A

beta chain D to J

207
Q

after heavy chain rearrangemnt check if its functional by

A

pairing with surrogate light chain (b cell) surrogate alpha cell (thymocyte)

208
Q

list steps for b cell rearrangemnt

A

pg 45/44 and go to previous ppts to get corect

209
Q

list steps for t cell rearrangemnt

A

pg 45/44 and go to previous ppts

210
Q

beta chain has to be able to pair with what to survive

A

surrogate light chain

211
Q

how many chances to rearrange beta chain

A

4 - two on each chromosome

212
Q

once you have heavy chain that works what do you do

A

allelic exclusion & proliferation - you have one that works keep it and make a lot of it

213
Q

follwoign proliferation of pre b or t cell

A

start rearranging nex thting, so alpha in thymocyte and l chain in B cell

214
Q

pre t cell needs to start expressing what after they rearrange the alph chain and stop expressing pre-T alpha

A

start expressing CD4 and CD8

will keep the one that work best and then get rid of the other

215
Q

surrogate chain is test of function for

A

first chain rearranged

216
Q

test ofr light chain is

A

heavy chain i nterms of b cells

see if it pairs with beta chain for TCR

217
Q

co-expression ofi IgM and IgD happens at what level

A

RNA - alternative splicing

218
Q

ability to secrete Ig is

A

RNA - alternativ splicing

219
Q

irrevirsible changes in b cell happen at

A

DNA level

220
Q

what happens in b cell that is irreversible change

A

pg 46

221
Q

once you switch from making igM to IgG you can’t

A

go back to making IgM b/c you’ve deleted the new gene segment from chromosome, but you cant switch to something downstream like IgA

222
Q

1st checkpoint for b and t cell

A

pre receptor

preBCR or preTCR

223
Q

second checkpoint in t and b cell development

A

second chain so light chain or alpha chain

224
Q

after 2nd checkpoint allows cells ot undergo

A

election

225
Q

when common lymphoid progenitor enter thymus and have notch ligand interaction they become first definable stage during t cell development and they do not express

A

CD4 or CD8

double negative

226
Q

signal for expression of CD4 and CD8 comes through

A

pre TCR signal

227
Q

following beta rearrangment and expresion f PreTCR you will start to express what on surface

A

CD4 and CD8

228
Q

after CD4 and CD8 will start to rearrange

A

alpha chain

229
Q

double positive cells will go onto

A

selection

230
Q

first part of selection happens where

A

cortex of thymus on surface of cortical epithelial cells

231
Q

cortical epithelial cells express

A

MHC I and MhC II

232
Q

if not interaction b/w MHC I and MHC II w/ t cell

A

t cell will die

233
Q

if TCR binds with high affinity to MHC presenting thymic peptide, what happens

A

t cell death

234
Q

outcome we want with TCR binding to thymic peptide

A

low affinity to MHC I or MHC II

235
Q

when TCR binds with low affinity it will

A

survive

236
Q

if TCR interacts with class I then

A

it wil be CD8

237
Q

if TCR interacts with class II then

A

it will be CD4

238
Q

CD3 signal maintains expression of what if TCR binds to MHC II

A

CD8 and loses expression fo CD4

239
Q

T cells arriv in medulla as

A

single positive - CD4 or CD8 not both

240
Q

if TCR recognized CD1d moelcule prsenting lipid r glycolipid they will

A

leave at that stage as double positive NKT cells

241
Q

most important negative selection for t cells location

A

medulla or boundary of medulla

242
Q

cells that mediste negativeselection in medulla that is most important negative selection

A

AIRE

243
Q

what does aire do

A

expresses celsl found elsewhere in the body so you can get rid of self reactive T cells

244
Q

CD4 t cells if there is intermediate affinity b/w TCR and mHC peptide complex then what happens

A

turns on expression of Foxp3 and becomes Treg

245
Q

what TF to become Treg

A

FOxp3

246
Q

Tregs that develop in thymus and in periphery are important for

A

silencing autoreactive t clls

247
Q

what is first pre or pro b

A

pro then pre b

248
Q

if BCR binds to self proteins then

A

there is opportunity to rescue BCR from autoreactivity by replacing light chain rearrangment with alternative light chainr earrangment

249
Q

how many chags to reararnge b cell light chain

A

lots!

250
Q

immature b cell stage can reactivate what

A

recombinase to try and replace the light chain rearrangement with alternative light chain to have it not be autoreactive or until you’ve used up all the J gene segments

251
Q

if b cell has used up all j segments and still autoreactive

A

death

252
Q

draw out an antibody

A

pg 50

253
Q

where is Fab on antibod

A

pg 50

254
Q

ends that interact with antigen

A

antigen binding site - include hypervariabl region

255
Q

Fc portion harbors

A

effector functions

256
Q

what is responsibel for acivating classical pathway of complement and what Fc receptor the IG can bind to

A

Fc portion

257
Q

Fab contains

A

variable region of heavy and light chain and first constant of heavy and only constant of light chain

258
Q

CDR1 and CDR2 are

A

encoded in VG segments in heavy and light chain

259
Q

CDR3 is generated through

A

joining

260
Q

constant domain in Fc portion determine

A

biological function

261
Q

most abundant Ig

A

IgG

262
Q

first antibody you wil make is

A

IgM

263
Q

during primary response you will switch to what isotype usually

A

IgG

264
Q

important function of IgG is

A

passive immunization of neonate due to placental transfer

265
Q

IgM structure

A

pentamer

266
Q

most Ig are what structure

A

monomer

267
Q

in circulation IgM is what structure

A

penatmer

268
Q

on cell surface IgM is what structure

A

monomer

269
Q

first Ig made during fetal development

A

IgM

270
Q

IgD structure

A

monomer

271
Q

IgD is found where

A

membrane bound on mature B cells

272
Q

IgA in ciruclation is what structure

A

monomer

273
Q

majority of IgA secreted as what in mucosa

A

dimer

274
Q

what holds two IgA together

A

J chain (I think?)

275
Q

lowerst Ig

A

IgE

276
Q

majority of IgE is

A

boudn to Fc epsiolon receptor on mast cells or basophils

277
Q

IgE important in what kind of response

A

allergic response and involves responses against parasites

278
Q

IgE structure

A

monomer

279
Q

mu heavy chain is what Ig

A

IgM

280
Q

what is most efficient isotype to activate complement

A

IgM

281
Q

why is IgM so good at activating complement

A

pentamer so only need one

282
Q

only Ig to cross placenta

A

IgG

283
Q

monomeric IgM binds with what affinity

A

low

284
Q

pentameric IgM affinty and avidity

A

low affinity but high avidity b/c there are so many of them

285
Q

IgG subclasses

A

1,2,3,4

286
Q

gamma is what Ig

A

IgG

287
Q

what IgG subclass is greatest amount

A

IgG1 (so IgG4 is lowest)

288
Q

once b cell switches to IgG BCR is

A

IgG

289
Q

best IgG sublcasses for complement activation

A

IgG1 and IgG3

290
Q

IgG is very important for

A

opsonization

291
Q

what IgG subclass poorest at crossing placenta

A

IgG2

292
Q

tapasin facilitates

A

putting peptides into MHC b/w α1 and α2

293
Q

explain MHC Class I pathway

A

Virus enter cell, replicates, get proteins that are made in cytosol, so the protein is made in our own cells cytosol, proteasome, chops the protein made by viral mRNA into pieces, peptide piece brought into ER, LHA class I with peptides will be expressed on surface

294
Q

explain MHC class II pathway

A

Big picture: infection, exracellular. Probalby bac. Take it in via endocytic vesicle, chop into pieces, miss with lysosome, bring MHC II and combine the two vesicles (one with pieces with MHC II) and express it on the outside. The origin of peptide was extracellular infection

295
Q

most abundant Ig we have not in serum

A

IgA but not in serum (but overall it is the most abundant we have)

296
Q

most important mucosal defense

A

IgA

297
Q

IgA subclasses

A

IgA 1 & 2

298
Q

what holds IgA dimer together

A

J chain

299
Q

what holds pentimer of IgM together

A

J chain

300
Q

heavy chain of IgA is

A

alpha 1 or alpha 2

301
Q

IgA1 can activate complement by what pathway

A

alternative & lectin

302
Q

IgA secreted across epithelial cells following binding of

A

pIgR via J chain

303
Q

heavy chain of IgE

A

epsilon

304
Q

minority of Ig in serum

A

IgE

305
Q

can IgE activate complement

A

no

306
Q

IgE can bind to high affinity Fcepsiolon receptors in absence of

A

antigen binding - which is how mast cells become senstized during hypersenstivity responses

307
Q

majority of IgE is boudn to

A

high affinity (Fcepsiolon) on mast cells and basophils and eosinophils

308
Q

IgE major role

A

parasitic infections and also associated with allergy

309
Q

what HSR is IGE associated with

A

HSR1

310
Q

heavy chain of IgD

A

delta

311
Q

can IgD activate complement

A

no

312
Q

main role of IgD

A

b cell receptor on mature naive b cells

313
Q

what kind of splicing leads to expression of IgD

A

RNA

314
Q

once t and b cells develop they go to

A

secondary lymph

315
Q

t cells go to where in lymph node

A

paracortex

316
Q

b cells go to where in lymph node

A

follicles

317
Q

antigen taken to lymph and can be taken what two ways

A

carried actively by dendritic cells

free in lymph fluid

318
Q

when dendritic cells take antigen to lymp h where do they take

A

paracortex

319
Q

when freel ymph carries antigen to lymph where does it take it

A

follicle & paracortex

320
Q

b cell zone and t cell zone are largely non-overlapping but you do find some t celsl in b zone area, which t cells

A

folliclular helper t cells

321
Q

if dendritic cell doesn’t find t cell to respond to it then it will

A

DIE

322
Q

if dendritic cell finds mhc to reognize what it is holding then it will

A

proliferate

323
Q

following signal 1 and 2 to t cell will get

A

clonal proliferation

324
Q

what IL drives proliferation of t cells

A

IL-2

325
Q

steps in adaptive t cell mediated immune response

A

Clonal selection - binding of APC by an antigen specific T cell, primarily in peripheral lymph organs
Signal 1 - APCs present peptide-MHC(Ag/MHC) to TCR on CD4+ T cells (T helper (Th) cells)
Signal 2 - APCs present co-stimulatory molecules to CD28 on T cell leading to IL-2 production and IL-2R expression
Clonal expansion - T cells are now receptive to autocrine (CD4+ T) and paracrine (CD8 T) stimulation by IL-2 leading to proliferation
Differentiation - T cells respond to cytokines to become effector and/or memory T cells

326
Q

what IL allows clonal expansion

A

IL02

327
Q

clonal expansion of CD4+ t cells is

A

autocrine

328
Q

clonal expansion of CD8 t cells is

A

paracrine

329
Q

after clonal expansino phase undifferentiated t cells are now receptive to signals that will

A

bias their differentiation into one of the CD subset

330
Q

Th0 is

A

uncommitted CD4 t cell

331
Q

cytokines bias to T-bet TF

A

IL-12 & IFN gamma

332
Q

T-bet promote differentiation into

A

Th1 cells

333
Q

Th1 cells secrete

A

IFN gamma

334
Q

IL-4 will turn on expression of what TF

A

GATA-3

335
Q

GATA-3 will differentiate into

A

Th2

336
Q

Th2 promote what immunity

A

humoral immunity

337
Q

Th1 promote what immunity

A

cel-mediated

338
Q

GATA-3 and Th2 esecrete

A

IL-4

339
Q

TGF beta will turn on expression of what TF

A

Foxp3

340
Q

Foxp3 will cause t cell to differentitate into

A

Treg

341
Q

Treg secrets

A

TGF beta and IL-10

342
Q

TGF beta and IL-6 turn on expression of what TF

A

RORgammat

343
Q

most pro-inflammatory subset

A

Th17

344
Q

RORgammat cuase t cell to differentiate into

A

Th17

345
Q

role of th17

A

pro-inflammatory

346
Q

Th17 secrete

A

IL-17

347
Q

key role of IL-2

A

Growth factor for Th0 cells and Th1 cells
Induces clonal proliferation Th0 cells
Secreted by Th0 cells and Th1 cells

348
Q

key role of IL-12

A

Induces differentiation of Th0 cells into Th1 cells

Produced by APC

349
Q

key role of IFN gamma

A

Induces differentiation of Th0 cells into Th1 cells
Inhibits proliferation of Th2 cells
Important for cell-mediated immunity (activates macrophages)
Produced by Th1 cells

350
Q

key role of IL-4

A 
Growth factor for Th2 cells
Inhibits proliferation of Th1 cells
Growth factor for B cells
Important for humoral immunity (stimulates antibody production)
Produced by Th2 cells
351
Q

how does Th1 cell activate macrophage

A

CD40L bind to CD40

IFN gamma bind to IFN gamma receptor

352
Q

Th1 how do they help for virus infections

A

they induce CTL differentiation (killer cells)

353
Q

if Th1 cell recognizes same antigen as a CTL cell then

A

Th1 will secrete IL-2 and then CTL be activated, now it can kill and will secrete perforin and granzymes

354
Q

key cytokine for promoting synthesis of perofrin and granzymes

A

IL-2

355
Q

how do you measure CTL or NK cell killing activity? what assay?

A

chromium release assay (chromium 51, following killing it will be released and measure the amoutn released which indicateds the amount of killing)

356
Q

review pg 69

A

69

357
Q

follwing activation t ell will express

A

CD40L but only briefly

358
Q

centorblasts

A

t cells that are actively rearranging VDJ

359
Q

extracellular pathogens need

A

high titer antibody response

360
Q

review pg 70

A

70

361
Q

review pg 71

A

Know cell type in innate response and adaptive response what will control the infection and what is inappropriate and would cause severe disease

362
Q

humoral immunity is

A

antibodies

363
Q

cell mediated

A

does not involve antibodies

364
Q

dipetheria

A

protein based subunit vaccine

365
Q

go to vaccine ppt we need to know different vaccines

A

you can do it

366
Q

MMR vaccine

A

measles, mumps, rubella

367
Q

type of vaccine MMR

A

live attenuated

368
Q

example natural passive immunization

A

transcplacental IgG

369
Q

purpose of subunit conjugate polysaccharide vaccines

A

generate t dependent response against polysacchardie
encapsulated bacteria surface is to polysacharide, cannot deal with them unless they are opsinized, so need IgG. isotype switching will not happen without t cell help, and t cells will not recognize polysaccharides

370
Q

active natural immunization

A

infectino

371
Q

active artifical imunization

A

vaccination

372
Q

isotype switching will not happen without

A

t cel lhelp

373
Q

name four live/attenuated vaccines

A

MMR
varicella
influenza
rotavirus

374
Q

name 2 inactivated/killed vaccines

A

polio (IPV)

hep A

375
Q

if you give someone inactivated poliovirus vaccine how will that be handeled by immune system after being taken up by dendritic cells

A

exogenous pathway b/c it’s inactivated so cross presentation pathway isn’t active
MHC II via exogenous pathway to CD4 t cells

376
Q

name a toxoid/inactivated toxin vaccine

A

dipehteria, tetanus

377
Q

name six subunit/conjugate vaccine

A 
hep b
influzna (injection)
Hib
pertussis
pneumonococcal
meningococcal
378
Q

review pg 74

A

74

379
Q

fastest type of rejection

A

pre-existing antibodies, hyperacute rejection

380
Q

antibodies that mediate hyperactue rejection are

A

easy to screen for

381
Q

most common form of graft rejection

A

acute rejection

382
Q

acute rejection usually mediated by

A

recipient t cells

383
Q

how long does acute rejection usually take

A

7-10 days

384
Q

if transplant rejected by acute rejection may need second transplant, if the second shared some MHC mismatches that were from the first one, then can get what direction

A

accelerated

385
Q

describe accelerated rejection of graft

A

memory response

386
Q

how many days for accelerated rejection

A

a few days

387
Q

what is cause of accelerated rejection of graft

A

reactivation (memory) pf sensitized t cells

388
Q

what is cause of graft versus host disease

A

Primary activation of donor T cells in transplanted bone marrow

389
Q

how long does GVHD take

A

days-weeks, minimum 7-10 days

390
Q

what cells are most important in preventing outgrowth of tumors

A

CD8+ CTL mediated lysis
CD4+ helper role
NK cell killing
Macrophages

391
Q

if macrophages infiltrate a solid tumor then they will turn into

A

immunosuppressant cells :(

392
Q

TSA is

A

antigen that is expressed by tumor cell but not any other cell regardless of stage of differentiation
mutations

393
Q

TSA stands for

A

tumor specific antigen

394
Q

E6 and E7 proteins of HPV in cervical cancer cells is that TSA or TAA

A

TSA

395
Q

TAA is

A

over-expressed normal proteins

396
Q

checmical/radiation induced cancers it at TSA or TAA

A

TS

397
Q

review pg 78

A

78

398
Q

if it is type IV the antibody is not pathogenic b/c

A

it is not humoral, it is cell mediated

399
Q

revie pg 79

A

79

400
Q

B27 strongly associated with

A

ankylosing spondylitis

401
Q

LADI is due to what deficiency

A

CD18

402
Q

LAD II due to what deficiency

A

CD15

403
Q

CGH due to what deficiency

A

NADPH oxidase

404
Q

susceptibility fo individuals with low levels of C3 and components of alternative pathway

A

encapsulated bacteria

405
Q

CHS is due to what deficiency

A

LYST

406
Q

C1, C2, C4 deficiencies predispose pt to

A

immune complex disease

407
Q

MAC deficiency (C5-9) susceptilbity to

A

neisseria infections

408
Q

mutations in PIGA gene (CD55 & CD59) gives rise to what disease

A

paroxysmal nocturnal hemoglobinuria

409
Q

C1-INH gives rise to what disease

A

Hereditary Angioedema (HAE)

410
Q

XLA genotype

A

Btk mutated

411
Q

XLA phenotype

A

no B cells

412
Q

X linked hyper IgM genotype

A

CD40L

413
Q

X linked hyper IgM phenotyep

A

no class witching, no GC

414
Q

AR hyper IgM genotype

A

AID deficiency

415
Q

AR hyper IgM phenotype

A

no class switching but giant germinal centers

416
Q

selective IgA deficiency genotype

A

unknown

417
Q

selective IgA phenotype

A

anti-IgA (especialky of IgE isotype)

418
Q

CVID genotype

A

various defects

419
Q

CVID phenotype

A

adolsescent, later onset

420
Q

selective IgG subclass deficiency genotype

A

defect uknown

421
Q

selective IgG sublcass def. phenotype

A

discvoered inadvertently

422
Q

clinical presentation of someone with omenn syndrome

A

SCID with eosinophilia

T cells that get out are useless

423
Q

DiGeroge syndrome phenotype

A

no thymus

thymic hypoplasia sometimes aplasia

424
Q

X linked proliferative syndrome clinical presentation?

A

cannot control viral infections, esp EBV

fulminant EBV infection

425
Q

Wiskott aldrich syndrome presentation?

A

classic triad:

ecezma

426
Q

ataxia telangiectasia associated with

A

IgA deficiency
difficulty walking
increase in serum levels of alpha beta protein

427
Q

multiple myeloma how would it present

A

pg 85 notecard

428
Q

notecard pg 86

A

86

429
Q

88

A

notecard pg 88

430
Q

notecard pg 89-94

A

yay

431
Q

describe conjjgate polysaccharide vaccine

A

have to link polysaccharide to peptide so b cell take it and be able to present to t celland can get cd4 t cell help and get t depdent antigen

Immunology Block 4 (10 decks)

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