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SFM Immunology > Final Exam > Flashcards

Final Exam Flashcards

To pass

1
Q

primary lymph

A

bone marrow, thymus

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2
Q

secondary lymph

A

spleen, lymph nodes, mucosal immune tissue

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3
Q

humoral components

A

Abs, complement, acute phase proteins

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4
Q

HPC

A

hematopoietic stem cell

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5
Q

HPC gives rise to

A

myeloid progenitors, lymphoid progenitors

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6
Q

myeloid cells originate from

A

bone marrow

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7
Q

G-CSF

A

granulocyte colony stimulating factor

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8
Q

M-CSF

A

monocyte stimulating factor

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9
Q

myeloid cells + G-CSF

A

myeloblast –> basophils, eosinophils, neutrophils (Grow, My BEN!)

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10
Q

myeloid cells + M-CSF

A

monoblast –> blood monocytes, dentritic cells (Make More Blood Money, Diamond Collector!)

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11
Q

lymphoid cells produce

A

T cells, B cells, NK cells

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12
Q

T cell precursor + IL-7 (thymus)

A

T lymphocytes

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13
Q

B cell precursor + IL-7 (bone marrow)

A

B lymphocytes

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14
Q

major leukocyte morphologies

A

granulocyte, mononuclear

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15
Q

granulocytes in the blood

A

basophils, eosinophils, neutrophils

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16
Q

granulocytes in the tissue

A

mast cells, tissue eosinophils

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17
Q

mononuclear cells in the blood

A

monocytes, T cells, B cells, NK cells

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18
Q

mononuclear cells in the tissue

A

macrophages, T lymphocytes, plasma cells, NK cells

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19
Q

phagocytic mononuclear cells

A

monocytes, macrophages, dendritic cells

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20
Q

in the tissue, monocytes produce

A

macrophages, dendritic cells

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21
Q

phagocytic granulocytes

A

neutrophils

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22
Q

what cells are indistinguishable on blood smear

A

mononuclear cells

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23
Q

CD

A

cluster of differentiation

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24
Q

how to distinguish mononuclear cells

A

CDs

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25
Q

T cell CD

A

CD3, CD4, CD8

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26
Q

B cell CD

A

CD19, CD20

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27
Q

NK cell CD

A

CD16, CD56

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28
Q

Monocyte CD

A

CD14

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29
Q

phagocytic cell types associated with innate immunity

A

neutrophils, macrophages, eosinophil (limited)

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30
Q

the professional phagocytes

A

neutrophils

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31
Q

granulocyte contents

A

peroxidase, lysozyme, degrative enzymes, defensins

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32
Q

defensin definition

A

Cys-rich, cationic, active against bacteria, fungi, viruses

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33
Q

neutrophils eliminate pathogens by

A

phagocytosis, degranulation, NETs

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34
Q

NETs

A

neutrophil extracellular traps

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35
Q

leukocytosis

A

elevated WBC count

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36
Q

largest component of WBC count

A

neutrophils

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37
Q

neutrophilia

A

elevated neutrophils

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38
Q

left shift

A

unmatured neutrophils present

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39
Q

neutrophil reserves located in

A

bone marrow

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40
Q

leukopenia

A

reduced WBC count

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41
Q

neutropenia, agranulocytosis, granulocytopenia

A

reduced neutrophils

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42
Q

professional APCs

A

DCs

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43
Q

mDCs

A

monocyte derived, responsible for capture, processing, and presentation of Ag to T cell

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44
Q

pDCs

A

IFN producing DCs in tissue and blood

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45
Q

Langerhans Cells (LCs)

A

DCs in epidermis

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46
Q

monocytosis

A

elevated monocytes

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47
Q

causes of monocytosis

A

chronic infections, autoimmune disorder, sarcoidosis

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48
Q

sarcoidosis

A

proliferation of resident macrophages

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49
Q

monocytopenia

A

reduced monocytes

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50
Q

bone tissue resident macrophages

A

osteoclasts

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51
Q

CNS tissue resident macrophages

A

microglial cells

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52
Q

lung tissue resident macrophages

A

alveolar macrophages

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53
Q

liver tissue resident macrophages

A

Kupffer cells

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54
Q

connective tissue resident macrophages

A

histiocytes

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55
Q

remodels tissue after inflammatory response

A

monocyte derived inflammatory tissue macrophages

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56
Q

defend against parasites

A

mast cells, basophils, eosinophils

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57
Q

mast cell granule contents

A

histamine, serotonin, heparin, cytokines, chemokines

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58
Q

normally emerges from bone marrow as immature cell

A

mast cells

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59
Q

matures locally

A

mast cells

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60
Q

sentinel cells definition

A

ubiquitous first defense cells

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61
Q

sentinel cell types

A

mast cells, DCs, tissue macrophages

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62
Q

mastocytosis

A

elevated mast cells

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63
Q

effects of histamine

A

itching, hives, anaphylactic shock

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64
Q

most common cutaneous mastocytosis

A

urticaria pigmentosa

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65
Q

eosinophil granule contents

A

histamine, peroxides, major basic protein

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66
Q

major basic protein associations

A

defense against helminths, atopic bronchospasm

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67
Q

eosinophilia

A

elevated eosinophils

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68
Q

causes of eosinophilia

A

parasites, atopic reaction

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69
Q

only lymphoid innate cells

A

NK cells

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70
Q

NK cell differentiation location

A

bone marrow

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71
Q

specificity of NK cell receptors

A

broad specificity

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72
Q

memory of NK cell response

A

does not exist

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73
Q

NK cell targets

A

neoplastic cells, infected cells

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74
Q

sebum components

A

lactic acid, fatty acids, low pH

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75
Q

microbial agents of milk

A

lactoperoxidase, lactoferrin, lysozymes

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76
Q

Ig found in mucous, tears, saliva, bronchial tissue

A

IgA

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77
Q

effects of vasodilators

A

contraction of nonvascular smooth muscle, increased vascular permeability, pain

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78
Q

pyrogenic cytokines

A

IL-1, TNFa, IL-6

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79
Q

target of pyrogenic cytokines

A

hypothalamus

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80
Q

PRRs

A

pattern recognition receptors

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81
Q

PAMPs

A

pathogen associated molecular patterns

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82
Q

pathogen evasion by alteration of PAMPs

A

does not exist

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83
Q

notable gram negative PAMP

A

LPS

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84
Q

notable gram positive PAMP

A

lipoteichoic acid

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85
Q

notable mycobacterial PAMP

A

lipoarabinomannan

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86
Q

notable fungal PAMP

A

beta-glucan

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87
Q

notable bacterial PAMP

A

terminal mannose

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88
Q

notable prokaryotic PAMP

A

fMET

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89
Q

PRR properties

A

germline encoded, nonclonal distribution

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90
Q

TLRs

A

toll-like receptors, type of PRR, activate inflammation

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91
Q

location of TLRs

A

cell surface, endosomes

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92
Q

cell surface TLRs recognize

A

extracellular PAMPs

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93
Q

endosomal TLRs recognize

A

nucleic acids

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94
Q

TLR1:TLR2 heterodimer

A

LPS (gram negative), GPI (parasites)

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95
Q

TLR2:TLR6 heterodimer

A

lipoteichoic acid (gram positive), zymosan (fungi)

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96
Q

TLR4:TLR4 homodimer

A

LPS (gram negative)

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97
Q

TLR5

A

flagellin (motile bacteria)

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98
Q

TLR3

A

dsDNA (virus)

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99
Q

TLR7

A

ssDNA (virus)

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100
Q

TLR8

A

viral ssRNA (virus)

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101
Q

TLR9

A

unmethylated CpG rich DNA (bacteria virus)

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102
Q

most important transcription factor for inflammation

A

NF-kB

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103
Q

NF-kB stimulates

A

acute inflammation, adaptive immunity

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104
Q

IRFs

A

interferon regulatory factors, transcription factors

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105
Q

IRFs stimulate

A

anti-viral cytokines IFNa/b

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106
Q

TLR adaptor proteins

A

MyD88, TRIF

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107
Q

MyD88 activates

A

IRAK-4 in TLR4 response to LPS (gram negative)

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108
Q

MyD88/IRAK-4 deficiency

A

susceptible to bacterial and viral infections

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109
Q

NLRs

A

NOD-like receptors

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110
Q

inflammasome

A

cytoplasmic complex containing NLRs

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111
Q

NLRs activate

A

NF-kB and MAPK pathways

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112
Q

most important NLR

A

NLRP3 in the cryopyrin inflammasome

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113
Q

NLRP3 activates

A

NF-kB pathway, caspase-1 mediated, secretion of proinflammatory IL-1b and IL-18

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114
Q

Key regulatory proinflammatory cytokine in gout

A

IL-1b

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115
Q

IL-1b promotes

A

neutrophil influx to synovium

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116
Q

NLRP3 associated DAMP

A

uric acid

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117
Q

gout anti-inflammatory therapy

A

anti IL-1b

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118
Q

DAMP

A

damage associated molecular pattern

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119
Q

DAMPs stimulate

A

NF-kB pathway, release of IL-1 and TNFa

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120
Q

DAMPs released by necrotic cells

A

HMGB1, uric acid, HSPs

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121
Q

HMGB1

A

DAMP, nucleolus protein

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122
Q

uric acid

A

DAMP, diffusible danger signal

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123
Q

HSPs

A

DAMP, cytoplasmic proteins

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124
Q

TLR2:TLR3 heterodimer

A

HMGB1

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125
Q

TLR2:TLR4 heterodimer

A

HSPs

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126
Q

autoimmune diseases associated with DAMPs

A

MS, type 1 DM, SLE, RA

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127
Q

PRR-triggered phagocytosis signals

A

formyl peptide receptor, mannose receptor

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128
Q

mast cells + IgE + Ag release

A

histamine

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129
Q

mast cells + PAMP release

A

proteases

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130
Q

mast cells + cytokine release

A

serotonin

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131
Q

mast cells + chemokines release

A

heparin

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132
Q

mast cells + C3a + C5a release

A

IL-4 and TNFa

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133
Q

controller of histamine and bradykinin

A

mast cells

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134
Q

mast cells are located in close proximity to

A

blood vessels

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135
Q

initial mast cell response

A

granule release (vasoactive amines), lipid-derived eicosanoid production

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136
Q

late-phase (2-24 hours after secondary exposure to allergen) mast cell response

A

vascular smooth contraction, endothelial vasodilation, leukocyte chemotaxis and activation

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137
Q

only innate immune cell that survives prolonged periods after activation

A

mast cells

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138
Q

cytokine molecule class

A

peptides

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139
Q

endocrine

A

long range

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140
Q

paracrine

A

short range

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141
Q

autocrine

A

itself and others

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142
Q

macrophages secrete all cytokines except

A

IFNg (secreted by NK cells and T cells to activate macrophages)

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143
Q

anti-inflammatory cytokines

A

IL-10, TGFb

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144
Q

IL-10

A

inhibits cytokine and chemokine production, reduces MHC-II production

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145
Q

TGFb

A

inhibits inflammation, differentiates Th17 and Treg

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146
Q

IL-8

A

neutrophils recruitment

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147
Q

IL-12

A

stimulates NK cells and T cells to release IFNg

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148
Q

C3b

A

opsonization, immune complex clearance

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149
Q

C3a, C5a

A

anaphylatoxin

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150
Q

anaphylatoxins cause release of

A

histamine

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151
Q

C5a

A

neutrophil recruitment

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152
Q

C3d

A

enhances immune response

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153
Q

MAC

A

membrane attack complex

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154
Q

MAC formation kills by

A

osmotic shock

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155
Q

AP

A

alternative pathway

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156
Q

CP

A

classical pathway

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157
Q

LP

A

lectin pathway

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158
Q

AP recognizes

A

microbes

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159
Q

CP recognizes

A

antibodies

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160
Q

LP recognizes

A

mannose binding lectin

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161
Q

CP: C1q binds

A

IgM or IgG (x2) on microbial surface

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162
Q

CP: C1r and C1s of the active C1qrs complex cleave

A

C2 and C4

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163
Q

CP: C4b covalently attaches to

A

microbial surface

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164
Q

CP: C2a binds

A

C4b (C4bC2a C3 convertase is formed)

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165
Q

CP: C3 convertase cleaves

A

C3

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166
Q

CP: C3b binds

A

microbial surface (C4bC2aC3b C5 convertase is formed)

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167
Q

CP: C5 convertase cleaves

A

C5

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168
Q

CP: C5b initiates

A

MAC self assembly

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169
Q

APPs

A

acute phase proteins

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170
Q

APPs act on

A

hepatocytes

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171
Q

major interleukins of APR

A

IL-6, IL-1, TNFa

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172
Q

APR

A

acute phase response

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173
Q

major APPs used to diagnose inflammation

A

CRP and SAA

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174
Q

where do neutrophils enter tissue from blood

A

post capillary venules

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175
Q

endothelial cells (ECs) activated by

A

IL-1 and TNFa from tissue resident macrophages

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176
Q

activated ECs upregulate

A

adhesion molecules P selectin (PS), E selectin (ES), ICAM-1, VCAM-1

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177
Q

adhesion ligands constitutively expressed on neutrophils

A

PSGL-1 and ESL-1 (static affinity), LFA-1 and VLA-1 (low affinity)

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178
Q

IL-8 is displayed on

A

ECs

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179
Q

IL-8 binding chemokine receptor of neutrophil activates

A

increased affinity of LFA-1 and VLA-4

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180
Q

rolling is dependent on

A

selectins

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181
Q

adhesion, crawling and transmigration are dependent on

A

integrins

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182
Q

most important chemoattractant for monocytes

A

MCP-1

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183
Q

classic (M1) macrophages activated by

A

PAMPs binding TLRs, IFNg

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184
Q

alternative (M2) macrophages activated by

A

IL-4 and IL-13

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185
Q

M1 macrophages

A

microbicidal, pro-inflammatory

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186
Q

M2 macrophages

A

wound repair, produce IL-10 and TGFb

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187
Q

M2 macrophage TGFb stimulates

A

myosin for wound contraction

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188
Q

NADPH oxidase

A

oxygen to superoxide

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189
Q

superoxide dismutase

A

superoxide to hydrogen peroxide

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190
Q

catalase

A

breaks down hydrogen peroxide

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191
Q

myeloperoxidase

A

hydrogen peroxide to hypochlorite

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192
Q

IFN-a/b

A

block viral replication, induce expression of protein kinase RNA (PKR) and ribonuclease L

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193
Q

PKR

A

prevents recycling of GDP (blocks RNA replication)

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194
Q

ribonuclease L

A

mediates viral RNA degradation)

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195
Q

type 1 interferons

A

IFN-a/b

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196
Q

IFN-a/b directly activate

A

NK cells

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197
Q

how activated NK cells take care of viruses

A

kill host cells, release intracellular contents for phagocytosis, secrete IFNg to activate macrophages

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198
Q

NK cell activating receptors (KARs)

A

recognize stress associated molecules on abnormal cell surfaces

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199
Q

KARs trigger activation of

A

protein tyrosine kinases (PTKs)

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200
Q

NK cell inhibitory receptors (KIRs)

A

recognize MHC-I on normal cell surfaces

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201
Q

KIR versus KAR, which signal is more important

A

sufficient KIR overrides KAR

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202
Q

NK cell granules contain

A

granzymes and perforins

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203
Q

alloantigen

A

tissue specific Ag present in one individual of a species but not in others (ABO, HLA)

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204
Q

epitope (antigenic determinant)

A

specific binding site of Ag

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205
Q

paratope

A

specific binding site of Ab or HLA

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206
Q

conformational determinant

A

recognition depends on shape

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207
Q

linear determinant

A

recognition depends on sequence

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208
Q

neoantigenic determinant

A

recognition depends on proteolysis

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209
Q

T-dependent Ag

A

protein recognized by TCR that stimulates T cell and B cell response

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210
Q

T-independent Ag

A

non-proteins recognized by BCR that stimulates B cell response

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211
Q

TCRs recognize

A

linear determinants of processed Ags presented by APCs

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212
Q

g/d T cells

A

recognize free peptides and lipids, reside in epithelial and mucosal compartments

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213
Q

immunodominant epitope

A

elicit T cell response

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214
Q

haptens

A

small molecules that cannot induce immune response alone

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215
Q

superantigens (SAgs)

A

not processed, bind directly to MHC-II and Vb chain of TCR

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216
Q

food poisoning SAg

A

Staphylococcal enterotoxins (SEA, SEB, SEC, SED, SEE)

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217
Q

toxic shock syndrome SAg

A

Staphylococcal toxic shock toxin (TSST-1)

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218
Q

scaled skin syndrome SAg

A

Streptococcal pyrogen exotoxins (shock)

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219
Q

general structure of Ab

A

four polypeptide chains held together by many disulfide bonds

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220
Q

heavy chains consist of

A

variable region (Fab) and constant region (Fc)

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221
Q

light chains consist of

A

variable region (Fab) and constant region (Fc)

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222
Q

classes of Abs

A

IgM, IgG, IgA, IgD, IgE of heavy chain Fab

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223
Q

types of Abs

A

kappa and lambda of light chain Fab

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224
Q

papain Ab digestion

A

branches of tree are removed, separating two Ag binding regions

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225
Q

pepsin Ab digestion

A

tree trunk is removed, leaving single bivalent binding capacity

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226
Q

each V domain has how many HV regions

A

three

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227
Q

each HV regions are flanked by how many FR regions

A

four

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228
Q

Ab allotype

A

allelic differences in C region of H chains

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229
Q

Ab idiotype

A

genetic differences in V region of H and L chains

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230
Q

first Ab produced in response to novel Ag

A

IgM

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231
Q

Ab pentamer

A

IgM

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232
Q

Ab efficient binding of C1 complex

A

IgM and IgG (x2)

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233
Q

Ab contains J piece that allows crossover to mucosa

A

IgM and IgA

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234
Q

Ab expressed on B cells as monomer

A

IgM and IgD

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235
Q

predominant Ab of secondary immune response

A

IgG

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236
Q

Ab which more and more produced with each secondary exposure

A

IgG

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237
Q

most abundant Ab in serum

A

IgG

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238
Q

differences between IgG subclasses

A

small structural differences on H chain

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239
Q

Abs of secondary immune response

A

IgG, IgA, IgE

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240
Q

Ab dimer

A

IgA

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241
Q

most abundant Ab in external secretions

A

IgA

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242
Q

Ab contains secretory component that binds Fc domains

A

IgA

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243
Q

bound to blood basophils and tissue mast cells by Fc receptor with high affinity

A

IgE

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244
Q

FcRn

A

recycles IgG across placental barrier after processing

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245
Q

types of interactions between Ag and Ag

A

hydrogen bonds, electrostatic bonds, van der Waals forces, hydrophobic forces

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246
Q

affinity

A

strength of interaction between univalent epitope and univalent paratope

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247
Q

avidity

A

strength of interaction between multivalent Ag and multivalent Ab

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248
Q

monoclonal Ab (mAb or moAb)

A

monospecific identical antibodies, all clones of single parent cell

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249
Q

zymogen

A

precursor enzyme

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250
Q

MAC C5b binds

A

C6 and C7

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251
Q

MAC C5bC6C7 complex attaches to

A

microbial membrane via C7

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252
Q

MAC C5bC6C7 complex attached to microbial membrane via C7 binds

A

C8, which then inserts itself into cell membrane

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253
Q

MAC C5bC6C7C8 complex binds

A

C9, which then polymerizes with 16 molecules of itself and forms a pore in the membrane

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254
Q

AP C3 “tickover”

A

spontaneous generation of C3a and C3b from C3

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255
Q

AP “tickover” C3b opsonizes microbial surface then binds

A

Factor B (FB)

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256
Q

AP FB (bound to C3b) cleaved by

A

Factor D (FD) (C3bBb C3 convertase is formed)

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257
Q

AP C3 convertase is enhanced and stabilized by

A

properdin

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258
Q

AP C3 convertase while stabilized by properdin binds

A

C3b (C3bBbC3b C5 convertase is formed)

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259
Q

compliment “amplification loop”

A

AP activated by C3b from CP or LP

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260
Q

CP: C1q binding Ab:Ag activates

A

C1r, which in turn activates C1s

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261
Q

LP: MBL attaches to

A

terminal mannose residues on microbial surface

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262
Q

LP: after attaching to microbial surface, MBL activates

A

MASP1 and MASP2

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263
Q

LP: activated MASP1 and MASP2 of MBL complex cleaves

A

C2 and C4, initiating cascade identical to CP

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264
Q

C1-INH inactivates

A

C1r and C1s, MASP1 and MASP2

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265
Q

DAF blocks interaction between

A

C4b and C2a

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266
Q

DAF prevents downstream assembly of

A

C3 and C5 convertases of CP and LP

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267
Q

Factor H (FH) binds

A

C3b

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268
Q

Factor H (FH) decay accelerating activity of

A

AP C3 and C5

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269
Q

Factor I (FI) degrades

A

C3b and C4b

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270
Q

Factor I (FI) destabilizes

A

C3 and C5 convertases of CP and LP

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271
Q

MAC inhibitory protein

A

CD59

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272
Q

CD59 blocks

A

C9 association with C5b-8 complex

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273
Q

C3a receptors are found on what type of cells

A

mast cells and basophils

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274
Q

C3a receptor binding induces

A

secretion of TNFa

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275
Q

C5a receptors are found on what type of cells

A

monocytes and macrophages

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276
Q

C5a receptor binding induces

A

secretion of IL-1, IL-6, prostaglandins, ROS, RON

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277
Q

most powerful anaphylatoxin of all complement proteins

A

C5a

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278
Q

CH50 measures

A

CP and LP

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279
Q

AH50 measures

A

AP and LP

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280
Q

low C3 and C4 indicate

A

chronic consumption in CS

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281
Q

mAb Comstatin

A

removes C3

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282
Q

mAb Eculizumab

A

removes C5

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283
Q

paroxysmal nocturnal hemoglobinuria (PNH) treatment

A

Comstatin and Eculizumab

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284
Q

HLA-I found on

A

all nucleated cells

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285
Q

HLA-II found on

A

macrophages, DCs, B cells, some thymocytes

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286
Q

HLA genes located on

A

chromosome 6

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287
Q

HLA-III influences the

A

inflammatory response

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288
Q

HLA haplotype

A

set of HLA alleles on each chromosome

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289
Q

HLA expression

A

codominant

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290
Q

HLA class I are designated with

A

single letters (A, B, C)

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291
Q

HLA class II are designated with

A

double letters (DMA, DMB, DOA)

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292
Q

HLA-I encoded by which three gene regions

A

HLA-A, HLA-B, HLA-C

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293
Q

HLA-I present to

A

TCR of CD8 CTL

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294
Q

HLA-I inhibitory receptor for

A

NK cells

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295
Q

HLA-I structure

A

heterodimer of a chain (a1, a2, a3 domains) and b2 chain

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296
Q

HLA-I peptide binding groove is located

A

between a1 and a2 domains of a chain

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297
Q

HLA-1 b2 binds a chain via

A

a3 domain

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298
Q

HLA-I peptide binding groove fits

A

peptides 8-10 amino acids in length

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299
Q

how many HLA-I alleles can be expressed in a given cell

A

all alleles expressed simultaneously

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300
Q

HLA-I a chain translated into what organelle

A

ER

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301
Q

in the ER, newly synthesized HLA-I a chain noncovalently interacts with

A

b2 chain

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302
Q

in the ER, newly synthesized HLA-I interacts with

A

peptides derived from cytosolic proteins

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303
Q

TAP

A

transfers cytosolic proteins into ER for association with HLA-I

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304
Q

HLA-II genes located in which region

A

HLA-D

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305
Q

HLA-II structure

A

a chain and b chain

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306
Q

HLA-D region encodes which chains of HLA-II

A

both a and b chains

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307
Q

how many HLA-II alleles can be expressed in a given cell

A

all of them

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308
Q

HLA-II peptide binding groove is located

A

between a1 and b1 domains of a and b chain

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309
Q

HLA-II peptide binding groove fits

A

peptides between 13 and 18 amino acids in length

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310
Q

which HLA peptide binding groove has open ends

A

HLA-II

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311
Q

how many peptides bind HLA

A

binds multiple different peptides (nonspecific) one at a time

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312
Q

HLA rate of “on rate” and “off rate”

A

slow “on rate”, very slow “off rate”

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313
Q

HLA peptide binding depends on what characteristic of peptide

A

size

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314
Q

TCR peptide binding depends on what characteristic of peptide

A

linear sequence (recognizes amino acid side chains)

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315
Q

H-Y antigen

A

antigens coded on Y chromosome associated with rejection of male grafts in female patients

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316
Q

CD4 binds what domain of HLA-II

A

b2

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317
Q

CD8 binds what domain of HLA-I

A

a3

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318
Q

phagocytic cell types associated with adaptive immunity

A

macrophages, DCs, B cells

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319
Q

DC phagocytic role in adaptive immunity

A

Ag presentation to naïve T cells

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320
Q

macrophage phagocytic role in adaptive immunity

A

Ag presentation to CD4 effector T cells during CMI

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321
Q

B cell phagocytic role in adaptive immunity

A

Ag presentation to CD4 helper T cells during humoral response

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322
Q

HLA-II expression in DCs and macrophages induced by

A

IFNg

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323
Q

costimulatory signal required during Ag presentation to T cell

A

CD40 from APC binding to CD40L on T cell

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324
Q

HLA-II expression in B cells induced by

A

IL-4

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325
Q

free Ags in the periphery are filtered by the

A

lymph and lymphoid tissue

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326
Q

free Ags in the blood are filtered by the

A

spleen

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327
Q

what cell types are located in spleen

A

macrophages and B cells

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328
Q

only cells that can activate naïve mature T cells

A

DCs

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329
Q

classic DCs produce which cytokines

A

TNFa, IL-6, IL-12, IL-23

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330
Q

classic DCs located in

A

all tissues

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331
Q

plasmacytodic DCs produce which cytokines

A

IFN-a/b

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332
Q

plasmacytodic DCs located in

A

blood and tissues

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333
Q

CCR7 expressed by

A

lymphatic endothelium

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334
Q

activated DCs increase expression of

A

B7/CD80

335
Q

HLA-II pathway processes what type of pathogens

A

extracellular`

336
Q

HLA-I pathway processes what type of pathogens

A

intracellular and self

337
Q

HLA-II a and b chains are produced in what organelle

A

ER

338
Q

where does extracellular pathogen processing take place

A

phagolysosome

339
Q

where is digested extracellular pathogen first introduced to HLA-II

A

late endosome

340
Q

invariant (Ii) chain prevents

A

HLA-II association with intracellular or self peptide in ER

341
Q

Ii degraded to

A

CLIP by lysosomal enzymes

342
Q

HLA-DM acts as a peptide exchanger in the late endosome during HLA-II processing, replacing

A

CLIP with extracellular antigen

343
Q

fate of unbound HLA-II molecules

A

not displayed

344
Q

intracellular or self proteins digested by

A

proteasome

345
Q

intracellular or self peptides transported into ER by

A

TAP

346
Q

posttranslational modification of cytosolic proteins destined for HLA-I pathway

A

ubiquitination

347
Q

what cell type can cross-present

A

DCs

348
Q

cross-presentation

A

DC uses both HLA-I for Ag presentation to CD8 CTL and HLA-II for Ag presentation to CD4 Th

349
Q

outcome of HLA-II Ag presentation to CD4 Th

A

promotes macrophage activation and B cell Ab secretion

350
Q

outcome of HLA-I Ag presentation to CD8 CTL

A

promotes killing of target cell

351
Q

HLA associated diseases

A

ankylosing spondylitis, rheumatic fever, Sjorgren’s syndrome, type 1 diabetes mellitus, psoriasis

352
Q

HLA associated with ankylosing spondylitis

A

HLA-B27 (HLA-I)

353
Q

HLA associated with rheumatic fever

A

HLA-DR4 (HLA-II)

354
Q

HLA associated with Sjorgren’s syndrome

A

HLA-DR3 (HLA-II)

355
Q

HLA associated with type I diabetes mellitus

A

HLA-DQw8 (HLA-II)

HLA-DRB1 (HLA-II)

356
Q

HLA associated with Psoriasis

A

HLA-B3 (HLA-I)

357
Q

Processing defect associated with renal cell carcinoma

A

downregulated TAP (HLA-I)

358
Q

Processing defect associated with bare lymphocyte syndrome class I

A

nonfunctional TAP (HLA-I)

359
Q

Processing defect associated with bare lymphocyte syndrome class II

A

defective transcription factor HLA-II transactivator (CIITA)

360
Q

CIITA induced by

A

IFNg

361
Q

RFX5, RFXAP, RFXANK are examples of

A

HLA-II transcription factors

362
Q

abnormal HLA-II or HLA-I expression results in

A

reduced T cell count due to failed thymic selection, reduced Ag presentation

363
Q

BCR structure

A

surface Ab and two invariant chains (Iga and Igb)

364
Q

part of BCR responsible for signal transduction

A

immunoreceptor tyrosine-base activation motif (ITAM) located on Iga and Igb

365
Q

TCR structure

A

heterodimer (a and b chains) associated with invariant CD3 complexes and homodimer (zeta chains)

366
Q

part of TCR responsible for signal transduction

A

immunoreceptor tyrosine-base activation motif (ITAM) located on CD3

367
Q

stem cell develops into

A

pro-lymphocyte

368
Q

pro-lymphocyte develops into

A

pre-lymphocyte

369
Q

pre-lymphocyte develops into

A

immature lymphocyte

370
Q

immature lymphocyte develops into

A

mature lymphocyte

371
Q

clonal selection occurs in the absence of

A

Ag

372
Q

which alleles can be expressed on BCR or TCR

A

only one allele per parent per cell (allelic exclusion)

373
Q

allelic exclusion

A

clones are monospecific

374
Q

combinatorial diversity

A

multiple genes for each region (germ line), multiple combinations of regions (somatic recombination)

375
Q

junctional diversity

A

additional nucleotides during process of D-J or V-DJ joining (H chain, b chain)

376
Q

somatic hypermutation

A

point mutations in fully assembled VJ and VDJ regions (occurs in H chain only)

377
Q

Ig H chain (M, D, G, A, E) B cell is equivalent to

A

b chain T cell

378
Q

Ig L chain (kappa, lambda) B cell is equivalent to

A

a chain T cell

379
Q

somatic hypermutation only occurs in

A

B cells (T cells are nonspecific)

380
Q

Ig H chain locus located

A

chromosome 14

381
Q

Ig L kappa chain locus located

A

chromosome 2

382
Q

Ig L lamda chain locus located

A

chromosome 22

383
Q

Ig H chain (TCR b chain) gene combination order

A

D-J, V-DJ

384
Q

Ig L chain (TCR a chain) gene combination order

A

V-J (no D domain in light chain)

385
Q

recombination signal sequences (RSSs)

A

ensure genes are combined in order (D-J before V-DJ)

386
Q

V(D)J recombinase recombines

A

V, D, J segments

387
Q

V(D)J recombinase activity initiated by

A

RAG1 and RAG2

388
Q

RAG1 and RAG2 are only expressed in

A

lymphocytes

389
Q

V(D)J recombinase tends to lose

A

nucleotides at sites of hairpin cleavage

390
Q

deoxyribonucleotidyl transferase (TdT) inserts

A

nucleotides between D and J segments

391
Q

P nucleotides added by TdT to

A

asymmetrically cleaved hairpins in templated manner

392
Q

N nucleotides added by TdT

A

in non-templated manner (random)

393
Q

TCR b chain locus located

A

chromosome 7

394
Q

TCR a chain locus located

A

chromosome 14

395
Q

TCR d chain locus located

A

chromosome 14 (remember g/d T cells)

396
Q

TCR g chain locus located

A

chromosome 7 (remember g/d T cells)

397
Q

B cell development location

A

bone marrow (mostly), spleen (not as much)

398
Q

stromal cell

A

connective tissue cell

399
Q

B cell development: B stem cells and bone stromal cells initially interact through

A

VCAM-1 (bone stromal cell) and VLA-4 (B stem cell), grows into early pro-B cell

400
Q

B cell development: VCAM-1 and VLA-4 promote interaction between

A

Kit (bone stromal cell) and SCF (B stem cell), grows into late pro-B cell

401
Q

B cell development: Kit-SCF interaction promotes

A

expression of IL-7 receptors, grows into pre-B cell

402
Q

B cell development: pre-B cell IL-7R stimulation by IL-7 results in

A

allelic exclusion of Ig H chain, production of surrogate chain, largest proliferative expansion

403
Q

B cell tolerance located

A

bone marrow

404
Q

B cell tolerance achieved when

A

immature B cell is not activated when challenged with self-Ag

405
Q

soluble self Ag: self-reactive immature B cells become

A

anergic

406
Q

B cell development: when fully processed BCR is expressed, the cell matures from pre-B cell to

A

immature B cell

407
Q

multivalent self Ag: self-reactive immature B cells become

A

deleted

408
Q

fate of anergic immature B cells

A

rescue by receptor editing of Ig L chain genes

409
Q

proteins required for anergic immature B cell rescue by receptor editing

A

RAG1 and RAG2

410
Q

immature lymphocyte rescue by receptor editing occurs in what cell types

A

only B cells

411
Q

T cell development location

A

progenitor T cells travel from bone marrow to develop in thymus

412
Q

thymocytes

A

immature T cells within the thymus

413
Q

how do progenitor T cells travel to the thymus

A

blood

414
Q

T cell development: pre-T cell IL-7R stimulation by IL-7 results in

A

allelic exclusion of b chain, production of surrogate chain, largest proliferative expansion, expression of CD4 and CD8

415
Q

T cell development: largest proliferative expansion located

A

thymic cortex

416
Q

positive selection of pre-T cells occurs in the

A

thymic cortex

417
Q

positive selection: thymocyte weak recognition of HLA-II presenting self-Ag

A

self-restricts to become CD4-only thymocyte

418
Q

positive selection: thymocyte weak recognition of HLA-I presenting self-Ag

A

self-restricts to become mature CD8-only thymocyte

419
Q

negative selection of self-restricted thymocytes occurs in the

A

thymic medulla

420
Q

negative selection: thymocyte strong recognition of either HLA-I or HLA-II presenting self-Ag

A

apoptosis

421
Q

negative selection: thymocyte fails to recognize HLA-I or HLA-II presenting self-Ag

A

death by neglect

422
Q

after positive and negative selection, the T cell is

A

mature, naïve

423
Q

Treg surface molecules

A

CD4, CD25 (high affinity IL-2R), CTLA-4

424
Q

Treg unique transcription factor

A

FOXP3

425
Q

mature naïve T cells surface molecules

A

CD4 or CD8, CD28, CD40L, HLA-I, TCR, LFA-1, VLA-4, CCR7

426
Q

mature naïve T cells enter peripheral lymph through high endothelial venules (HEV) by

A

weak adhesion (L-selectin binds L-selectin ligand of HEV) followed by stable arrest (LFA-1 binds ICAM-1 of HEV)

427
Q

first signal between APC and T cell

A

HLA/Ag binds TCR

428
Q

second signals between APC and T cell

A

CD40 (APC) binds CD40L (T cell), B7 (APC) binds CD28 (T cells)

429
Q

first and second signals between APC and T cell stimulate APC to release

A

IL-12 to enhance T cell activation

430
Q

activation of TCR CD3 ITAMs results in

A

Lck (kinase on CD4 and CD8) activates ZAP-70 (tyrosine kinase on zeta chains)

431
Q

transcription factors stimulated after TCR activation

A

NF-kB, NFAT, AP-1

432
Q

TCR activation and NF-kB, NFAT, AP-1 production increases: transcription factors

A

c-Fos and c-Myc

433
Q

TCR activation and NF-kB, NFAT, AP-1 production increases: increase membrane effectors

A

CD40L and FasL

434
Q

TCR activation and NF-kB, NFAT, AP-1 production increases: cytokines

A

IL-2, IFNg, IL-4

435
Q

TCR activation and NF-kB, NFAT, AP-1 production increases: cytokine receptors

A

CD25 (IL-2Ra)

436
Q

induction of anergy in mature T cells

A

HLA/Ag without costimulatory signals

437
Q

IL-2

A

T cell proliferation, Treg survival

438
Q

IL-2Rbgc

A

low affinity

439
Q

IL-2Ra (CD25)

A

high affinity

440
Q

B7 (APC) binding CD28 (T cells) induces

A

a chain addition to IL-2R to increase affinity

441
Q

IL-4

A

IgE class switching

442
Q

IL-5

A

IgA class switching, eosinophil activation

443
Q

IL-17

A

proinflammatory

444
Q

IL-22

A

neutrophil recruitment

445
Q

IFNg

A

activates macrophages

446
Q

Ag-specific T cells are arrested in lymph nodes by

A

CD69

447
Q

CD69 binds

A

S1PR of lymph node

448
Q

IFN-a/b promotes or inhibits CD69 membrane fusion to S1PR of lymph node?

A

promotes

449
Q

S1P promotes or inhibits CD69 membrane fusion to S1PR of lymph node?

A

inhibits (sequesters S1PR)

450
Q

time to Ag recognition by Ag-specific T cell arrested in lymph node

A

2 days

451
Q

time to Ag-specific T cell activation in lymph node and response to Ag arrival

A

5 days

452
Q

CD4 T cell + IFNg + IL-12

A

Th1

453
Q

Th1 defends against

A

intracellular pathogens

454
Q

Th1 secretes

A

TNFa, IFNg, IL-2 to activate classical macrophages, CTLs, and NK cells

455
Q

CD4 T cell + IL-4

A

Th2

456
Q

Th2 defends against

A

extracellular pathogens (helminths)

457
Q

Th2 secretes

A

IL-4, IL-5, IL-13 to activate eosinophils, mast cells, and alternative macrophages

458
Q

CD4 T cell + IL-1 + IL-6

A

Th17

459
Q

T follicular helper (Tfh) cells defend against

A

extracellular pathogens by helping B cell development

460
Q

Tfh cell activation occurs in

A

medullary area in lymph node

461
Q

activated Tfh cells migrate to

A

edge of follicular zone in lymph node

462
Q

activated Tfh cells increase expression of surface protein

A

CTLA-4 (makes APCs tolerant by binding B7)

463
Q

activated Tfh cells secrete

A

IL-21 and either IFNg or IL-4

464
Q

naïve B cell + LPS + IL-4

A

IgG and IgE

465
Q

naïve B cell + LPS + TGFb

A

IgG and IgA

466
Q

Treg cells activated by

A

TGFb and IL-2

467
Q

activated Treg cells secrete

A

TGFb, IL-10, IL-4

468
Q

CTLA-4 (Tregs) binds B7 (APCs) more avidly than

A

CD28 (T cells)

469
Q

Th1 novel transcription factor

A

T-bet

470
Q

activated classical (M1) macrophage secretes

A

IL-1, TNFa, IL-12

471
Q

Th2 novel transcription factor

A

GATA-3

472
Q

activated alternative (M2) macrophage secretes

A

TGFb and IL-10

473
Q

activated Th17 cells secrete

A

IL-17 and IL-22

474
Q

Th17 novel transcription factor

A

RORgt

475
Q

will every effector T cell that enters an area be specific for Ag

A

no (selectins and integrins are nonspecific)

476
Q

location of CD8 CTL activation

A

peripheral tissue

477
Q

location of CD4 Th cell activation

A

lymph

478
Q

CD8 CTLs release what onto surface of target cells

A

preformed lytic granule containing perforin and granzymes

479
Q

CD8 CTLs and target cell interaction is stabilized by

A

ICAM-1 (target) binding LFA-1 (CTL)

480
Q

CD8 CTLs induces apoptosis of target cell by

A

CD95/Fas (target) binding FasL (CTL)

481
Q

NK cell killing enhanced by

A

IL-12 and IFN-a/b

482
Q

NK cell killing inhibited by

A

HLA-I

483
Q

ADCC

A

Ab-dependent cell-mediated cellular cytotoxicity

484
Q

ADCC associated Abs

A

IgG or IgE binds to target cell

485
Q

ADCC associated killers

A

NK cells, macrophages, monocytes, neutrophils, eosinophils (granular cells)

486
Q

T memory cells remain after contraction of immune response because they express increased levels of

A

Bcl-2

487
Q

T memory cells require what cytokines for survival

A

IL-7 and IL-15

488
Q

regulatory receptors of adaptive immunity

A

CTLA-4 and PD-1

489
Q

CTLA-4 (activated T cells)

A

binds B7 on APCs and induces anergy (tolerance)

490
Q

PD-1 (T cells, B cells, myeloid cells)

A

binds PDL on APCs, tumor cells

491
Q

T cell exhaustion occurs

A

during chronic infection, when CTLA-4 and PD-1 induced

492
Q

mycobacteria evasion mechanism

A

survive within phagosome

493
Q

HSV and CMV evasion mechanisms

A

inhibition of Ag presentation

494
Q

EBV evasion mechanisms

A

inhibition of Ag presentation, secretion of IL-10

495
Q

pox virus evasion mechanisms

A

block cytokine activation of effector cells

496
Q

T cell surface molecules

A

TCR, CD4 or CD8, CD3, CD28, CTLA-4, PD-1, L-selectin, LFA-1, CCR7, CD40L

497
Q

B cell surface molecules

A

BCR, co-BCR (CD19, CD21), HLA-II, CD40, B7, CD20, ICAM-1, CXCR5

498
Q

mature naïve BCR

A

IgM, IgD, Iga and Igb)

499
Q

B1 cells located

A

mucosa, limited Ag specificity, T-independently activated

500
Q

B2 cells are divided into

A

follicular and marginal

501
Q

follicular B cells located

A

primary and secondary lymph, T-dependently activated

502
Q

marginal B cells located

A

spleen, recognize blood born polysaccharide Ags, T-independently activated

503
Q

activation of mature naïve B cell in circulation prompts travel to

A

secondary lymphoid tissue (SLT) where they enter and travel to primary follicle (lymph node)

504
Q

FDCs

A

B cell survival signals

505
Q

first signal for B cell activation (T-dependent or T-independent)

A

crosslinking of 2 or more BCR by Ag

506
Q

first signal for B cell activation (T-dependent or T-independent) stimulates secretion of

A

IgM

507
Q

first signal for B cell activation (T-dependent or T-independent) signaling occurs through

A

Iga and Igb, CD21/CR2, CD19 cytoplasmic tails and involves Syk-B cell phosphorylation

508
Q

compared to Ag bound with C3d, unbound Ag is

A

less immunogenic

509
Q

first signal for B cell activation (T-dependent or T-independent) results in synthesis of

A

transcription factors Myc, NFAT, NF-kB, AP-1

510
Q

after the first signal and before the second signal during T-dependent B cell activation, B cells increase CCR7 and migrate to

A

edge of follicular zone then enter T cell zone

511
Q

CXCR5

A

how T cells locate primary follicles

512
Q

T-independent second signal for B cell activation

A

mitogenic stimulation of B cell by Tl-1 antigen (TLRs recognizing PAMPs)

513
Q

T-dependent second signal for B cell activation

A

co-stimulation between Th cell (CD40L) and B cell (CD40)

514
Q

what cells are found in the germinal centers

A

activated B cells, Tfh cells, follicular DCs

515
Q

Tfh in the germinal center secrete

A

IL-21, IFNg, IL-4

516
Q

IL-21 secreted by Tfh cells facilitates

A

B cell differentiation to plasmablasts

517
Q

Tfh cell cytokines induce

A

H chain class switching and affinity maturation

518
Q

Tfh cell cytokines H chain class switching and affinity maturation by increasing expression of

A

activation-induced deaminase (AID)

519
Q

AID

A

converts C’s to Us by deamination, allowing AP endonuclease to create double strand breaks

520
Q

Tfh cell surface molecules

A

CD4, low levels of CD25 (IL-2Ra), ICOS

521
Q

in the T cell zone, Tfh cells and activated B cells interact by

A

ICOS (Tfh cell) binds ICOS-L (activated B cell)

522
Q

after ICOS-ICOSL interaction occurs, activated B cell and Tfh cell migrate back to

A

follicular area and establish germinal centers

523
Q

B cells producing highest affinity Abs are selected for survival through

A

FDC and Tfh interactions

524
Q

what organelle is enlarged in plasma cells

A

ER

525
Q

plasma cell surface molecules

A

high CD27, low CD19, CD20, HLA-II

526
Q

do T-dependently activated or T-independently activated plasma cells live longer

A

T-dependently activated plasma cells live longer

527
Q

affinity and isotype of T-independently activated plasma cells

A

mainly IgM, low-affinity

528
Q

affinity and isotype of T-dependently activated plasma cells

A

isotype-switched, high-affinity

529
Q

plasma cells are active during

A

primary response

530
Q

memory cells are active during

A

secondary response

531
Q

B memory cells remain after contraction of immune response because they express increased levels of

A

Bcl-2

532
Q

B memory cell surface molecules

A

CD27, CD45R(O)

533
Q

primary response lag after immunization

A

5-10 days

534
Q

primary response Ab class

A

IgM > IgG

535
Q

primary response Ab affinity

A

low (no affinity maturation)

536
Q

secondary response lag after immunization

A

1-3 days

537
Q

secondary response Ab class

A

increased IgG, and under certain circumstances, IgA or IgE

538
Q

secondary response Ab affinity

A

high (affinity maturation)

539
Q

most important cell for Ab production during humoral active immune response

A

plasma cells

540
Q

plasma cell location

A

lymph

541
Q

effector function of Abs mediated by what region of molecule

A

Fc

542
Q

what are the five effector functions of Abs

A

neutralization, opsonization, ADCC, inflammation, CS activation, lysis (NO, ADCC, CSAL)

543
Q

CD32/FcgRIIb

A

high affinity, B cells and sentinel cells, Ab feedback and attenuation of inflammation

544
Q

Ab feedback

A

negative feedback for IgG only

545
Q

Ab feedback: BCR signaling leads to formation of

A

PIP3

546
Q

Ab feedback: Ab/IgG complex binds CD32/FcgRIIb which converts

A

PIP3 to PIP2

547
Q

CD16/FcgRIIIa

A

high affinity, NK cells, ADCC

548
Q

CD64/FcgRI

A

low affinity, phagocytes, activates phagocytosis

549
Q

FceRI

A

low affinity, granulocytes, activates degranulation

550
Q

what classes of Abs neutralize

A

all classes of Abs neutralize

551
Q

what effector function of Abs sterically hinders microbes and toxins

A

neutralization

552
Q

what effector function of Abs allows for clearance of immune complexes (ICs)

A

opsonization

553
Q

erythrocyte CD64/FcgRI binds

A

circulating ICs then transports to liver and spleen where organ resident phagocytes remove IC from surface

554
Q

purpose of IVIG therapy in autoimmune disease

A

provide passive immunity while engaging inhibitory FcR on B cells (IgG negative feedback)

555
Q

anti-venom is an example of

A

passive immunization

556
Q

natural exposure and vaccines are examples of

A

active immunization

557
Q

does passive or active create immunologic memory

A

active

558
Q

pros and cons of passive immunity

A

immediate but transient

559
Q

pros and cons of active immunity

A

delayed but lasting

560
Q

tetanus and rabies immunizations are examples of

A

combined passive-active immunization

561
Q

influenza and HIV evasion of humoral immunity

A

antigenic variation

562
Q

Neisseria gonorrhea evasion of humoral immunity

A

inhibition of complement activation

563
Q

Streptococcus evasion of humoral immunity

A

hyaluronic acid capsule blocking T cell CD44 binding, Ab binding, and phagocytosis

564
Q

hyperplasia of germinal centers suggests

A

normal B cell development

565
Q

absence of secondary follicles and germinal centers suggests

A

abnormal B cell development

566
Q

challenge of previous vaccine tests ability to elicit

A

secondary immune response

567
Q

challenge of novel vaccine tests ability to elicit

A

primary immune response

568
Q

most important Ig for pyogenic bacterial defense

A

IgG

569
Q

Cyclosporin A inhibits

A

CD40L

570
Q

Tuberculoid leprosy

A

Th1 favored, low infectivity, granulomas and local inflammation, peripheral nerve damage

571
Q

Lepromatous leprosy

A

Th2 favored, high infectivity, disseminated infection

572
Q

screen humoral immunity for

A

recurrent sinopulmonary bacterial infections

573
Q

screen cellular immunity for

A

recurrent viral and/or fungal infection

574
Q

screen phagocytes for

A

recurrent skin abscesses and/or fungal infections

575
Q

screen complement for

A

bacteremia or meningitis with encapsulated bacteria

576
Q

Diff CBC screens for

A

T cell, B cell, T/B cell defects

577
Q

DTH skin test screens for

A

T cell defects (negative = impaired T cell response)

578
Q

serum Ig screens for

A

humoral immunodeficiency

579
Q

total hemolytic complement assay screens for

A

complement deficiency

580
Q

nitroblue tetrazolium test screens for

A

phagocytic disorder

581
Q

selective T cell immunodeficiencies

A

common gamma chain, IL-7R alpha chain, BLS II, MHC class I, CD3, DiGeorge syndrome

582
Q

selective B cell immunodeficiencies

A

BTK agammaglobulinemia, agammaglobulinemia, IgA, IgG subclass, HIGM syndrome, transient hyper-IgM

583
Q

severe combined immunodeficiencies (SCIDs)

A

ADA, PNP, artemis, RAG1/RAG2, Jak3

584
Q

ADA immunophenotype

A

T- B- NK-

585
Q

ADA Ab panel

A

IgM- IgG- IgA-

586
Q

SCID infections

A

severe opportunistic

587
Q

SCID vaccination

A

no live vaccines

588
Q

PNP immunophenotype

A

T- B- NK-/+

589
Q

PNP Ab panel

A

often normal

590
Q

artemis immunophenotype

A

T- B- NK+

591
Q

artemis Ab panel

A

some mutations can be low

592
Q

SCID inheritance

A

autosomal

593
Q

RAG1/RAG2 immunophenotype

A

T- B- NK+

594
Q

RAG1/RAG2 Ab panel

A

IgM- IgG- IgA-

595
Q

Jak3 immunophenotype

A

T- B+ NK-

596
Q

Jak3 Ab panel

A

IgM+ IgG- IgA-

597
Q

BTK agammaglobulinemia immunophenotype

A

T+ B- NK+

598
Q

BTK agammaglobulinemia Ab panel

A

IgM- IgG- IgA-

599
Q

BTK agammaglobulinemia inheritance

A

X-linked

600
Q

BTK agammaglobulinemia infections

A

recurrent bacterial

601
Q

BTK agammaglobulinemia vaccination

A

no live vaccines

602
Q

agammaglobulinemia immunophenotype

A

T+ B- NK+

603
Q

agammaglobulinemia Ab panel

A

IgM- IgG- IgA-

604
Q

agammaglobulinemia inheritance

A

autosomal

605
Q

agammaglobulinemia infections

A

recurrent bacterial

606
Q

agammaglobulinemia vaccination

A

no live vaccines

607
Q

IgA immunophenotype

A

T+ B+ NK+

608
Q

IgA Ab panel

A

IgM+ IgG+ IgA-

609
Q

IgA inheritance

A

autosomal higher in male

610
Q

IgA infections

A

mostly asymptomatic

611
Q

IgA vaccinations

A

no restrictions

612
Q

IgG subclass immunophenotype

A

T+ B+ NK+

613
Q

IgG subclass Ab panel

A

IgM+ IgG+ IgA+

614
Q

IgG subclass inheritance

A

autosomal

615
Q

IgG subclass infections

A

mostly asymptomatic

616
Q

IgG subclass vaccination

A

no restrictions

617
Q

HIGM immunophenotype

A

T+ B+ NK+

618
Q

HIGM Ab panel

A

IgM+ IgG- IgA-

619
Q

HIGM inheritance

A

X-linked and autosomal

620
Q

HIGM infections

A

encapsulated opportunistic

621
Q

transient HIGM immunophenotype

A

T+ B-/+ NK+

622
Q

transient HIGM Ab panel

A

IgM+ IgG- IgA-

623
Q

transient HIGM inheritance

A

N/A

624
Q

transient HIGM infections

A

encapsulated opportunistic

625
Q

transient HIGM vaccination

A

POLIO not recommended

626
Q

HIGM vaccination

A

POLIO not recommended

627
Q

common gamma chain immunophenotype

A

T- B+ NK-

628
Q

common gamma chain Ab panel

A

IgM+ IgG- IgA-

629
Q

common gamma chain inheritance

A

X-linked

630
Q

common gamma chain infections

A

severe opportunistic infections

631
Q

common gamma chain vaccination

A

no live vaccines

632
Q

IL-7Ra chain immunophenotype

A

T- B+ NK+

633
Q

IL-7Ra chain Ab panel

A

IgM+ IgG- IgA-

634
Q

IL-7Ra chain inheritance

A

autosomal recessive

635
Q

IL-7Ra chain infections

A

severe opportunistic

636
Q

IL-7Ra chain vaccination

A

no live vaccines

637
Q

BLS II immunophenotype

A

CD4 lymphopenia

638
Q

BLS II Ab panel

A

hypogammaglobulinemia

639
Q

BLS II inheritance

A

autosomal recessive

640
Q

BLS II infections

A

severe opportunistic

641
Q

BLS II vaccinations

A

no live vaccines

642
Q

MHC class I immunophenotype

A

CD8 lymphopenia, functional NK deficiency

643
Q

MHC class I Ab panel

A

IgM+ IgG+ IgA+

644
Q

MHC class I inheritance

A

autosomal recessive

645
Q

MHC class I infections

A

recurrent viral

646
Q

MHC class I vaccination

A

no restrictions

647
Q

CD3 immunophenotype

A

T- B+ NK+

648
Q

CD3 Ab panel

A

IgM+ IgG- IgA-

649
Q

CD3 inheritance

A

autosomal recessive

650
Q

CD3 infections

A

recurrent viral

651
Q

CD3 vaccination

A

no live vaccines

652
Q

DiGeorge syndrome immunophenotype

A

T- B+ NK+

653
Q

DiGeorge syndrome Ab panel

A

usually normal

654
Q

DiGeorge syndrome inheritance

A

autosomal dominant

655
Q

DiGeorge syndrome infections

A

recurrent viral

656
Q

DiGeorge syndrome vaccination

A

no restrictions

657
Q

adenosine deaminase (ADA)

A

deoxyadenosine accumulation

658
Q

purine nucleoside phosphorylase (PNP)

A

dGTP accumulation

659
Q

artemis

A

VDJ recombinase, repairs double strand breaks

660
Q

artemis red flags

A

radiosensitivity, lymphoma

661
Q

RAG1/RAG2

A

modulate initiation of VDJ recombinase

662
Q

Omenn syndrome

A

partial functioning RAG1/RAG2, eosinophilia and high IgE

663
Q

BTK

A

rearranges Ig H chain

664
Q

IgA red flags

A

non-IgE mediated anaphylaxis in response to IVIG

665
Q

DiGeorge microdeletion of

A

22q11.2 region

666
Q

DiGeorge red flags

A

cardiac anomalies, hypocalcemia, hypoplastic thymus

667
Q

live viral vaccine CD8 T cell cut off

A

> 300 cells/mm3

668
Q

HIGM

A

impaired class switching

669
Q

transient hypogammaglobulinemia of infancy immunophenotype

A

T+ B+ NK+

670
Q

transient hypogammaglobulinemia of infancy Ab panel

A

hypogammaglobulinemia, IgM low or normal

671
Q

common variable immune deficiency (CVID) immunophenotype

A

T+ B-/+ NK+

672
Q

common variable immune deficiency (CVID) Ab panel

A

hypogammaglobulinema, IgM low or nomal

673
Q

transient hypogammaglobulinemia of infancy age range

A

resolves 2-4 years of age

674
Q

common variable immune deficiency (CVID) age range

A

diagnosed 20-30 years of age

675
Q

common gamma chain receptor

A

IL-2Rg

676
Q

B cells in common gamma chain deficiency

A

present but not functional since T cells are unable to proliferate

677
Q

B cells in IL-7Ra chain deficiency

A

present but not functional since T cells are unable to proliferate

678
Q

Th1 cell deficiency mutation

A

IL-12, IL-12R, IFNgR

679
Q

Th1 cell deficiency cannot produce

A

IFNg

680
Q

Th17 deficiency due to mutations in

A

IL-17, IL-17R, STAT1, STAT3, AIRE

681
Q

Th17 deficiency red flags

A

atopic disease, chronic mucocutaneous candidiasis, recurrent Staphylococcus aureus

682
Q

IPEX mutation

A

FOXP3

683
Q

IPEX results in

A

loss of inhibition of Treg

684
Q

ALPS mutation

A

Fas, FasL, caspase-8, caspase-10

685
Q

ALPS results in

A

no DISC formation, resistance of effector T cell to apoptosis

686
Q

WAS mutation

A

WASP

687
Q

WAS immunophenotype

A

T- B+ NK-

688
Q

WAS Ab panel

A

low IgM, normal IgG, high IgA and IgE

689
Q

WAS inheritance

A

X-linked

690
Q

classical NK cell deficiency (CNKD)

A

absence of NK cells

691
Q

classical NK cell deficiency (CNKD) mutation

A

GATA2

692
Q

functional NK cell deficiency (FNKD)

A

presence of defective NK cells

693
Q

functional NK cell deficiency (FNKD) mutation

A

perforin

694
Q

leukocyte adhesion deficiency (LAD) mutation

A

CD18

695
Q

leukocyte adhesion deficiency (LAD) results in

A

defective migration of phagocytes into infected tissues

696
Q

leukocyte adhesion deficiency (LAD) infections

A

encapsulated bacteria

697
Q

chronic granulomatous disease (CGD) mutation

A

NADPH oxidase, phagocytes cannot produce superoxide

698
Q

chronic granulomatous disease (CGD) results in

A

impaired killing of phagocytosed bacteria

699
Q

chronic granulomatous disease (CGD) infections

A

catalase-positive organisms, granulomas

700
Q

G6PD deficiency mutation

A

G6PD, defective respiratory burst

701
Q

G6PD deficiency results in

A

impaired killing of phagocytosed bacteria

702
Q

G6PD deficiency infections

A

chronic bacterial and fungal, anemia induced by certain medication, granulomas

703
Q

myeloperoxidase deficiency mutation

A

myeloperoxidase, phagocytes cannot produce toxic oxygen species

704
Q

myeloperoxidase deficiency results in

A

impaired killing of phagocytosed bacteria

705
Q

myeloperoxidase deficiency infections

A

chronic bacterial and fungal

706
Q

Chediak-Higashi syndrome mutation

A

cathepsin G and elastase, defect in vesicle fusion

707
Q

Chediak-Higashi syndrome results in

A

impaired phagocytosis due to inability of endosomes to fuse lysosomes

708
Q

Chediak-Higashi syndrome infections

A

recurrent pyogenic granulomas

709
Q

granuloma

A

mass of immune cells at site of inflammation or infection

710
Q

CGD inheritance

A

autosomal, more common in males

711
Q

G6PD inheritance

A

X-linked

712
Q

LAD red flags

A

neutrophilia, inability to form pus, delayed detachment of umbilical cord

713
Q

Chediak-Higashi syndrome red flags

A

azurophilic giant cytoplasmic inclusions in blood cells, partial albinism, absent NK activity

714
Q

CP: C1 and C4 deficiency associated with

A

SLE or RA

715
Q

CP: C2 deficiency red flags

A

recurrent Streptococcus pneumoniae

716
Q

C5-C9 deficiency red flags

A

recurrent Neisseria infections

717
Q

absent C8 in presence of normal C3 and C4 suggests

A

C8 deficiency

718
Q

absent C8 in presence of low C3 and C4 suggests

A

chronic complement consumption

719
Q

AP: properdin, FB, FD deficiency red flags

A

Neisseria meningitis and other extracellular bacteria

720
Q

AP: FH deficiency associated with

A

hemolytic uremic syndrome or glomerulonephritis

721
Q

AP: C1-INH deficiency associated with

A

hereditary angioedema (HAE)

722
Q

AP: C1-INH mutation

A

SERPING1 gene

723
Q

AP: DAF deficiency associated with

A

paroxysmal nocturnal hemoglobinuria (PNH)

724
Q

AP: DAF deficiency mutation

A

GPI anchor

725
Q

most important GPI anchor proteins

A

CD55/DAF and CD59/MIRL

726
Q

MyD88 deficiency results in

A

impaired signaling for all TLRs except TLR3

727
Q

MyD88 infections

A

pyogenic pacteria

728
Q

MyD88 red flags

A

afebrile, normal ESR/CRP, low IL-1, TNFa, IL-6

729
Q

TLR3 deficiency inheritance

A

autosomal dominant

730
Q

TLR3 deficiency results in

A

increased susceptibility to HSV encephalitis

731
Q

development of central tolerance located

A

primary lymphoid organs

732
Q

central tolerance is induced in

A

immature self-reactive lymphocytes

733
Q

development of peripheral tolerance located

A

lymph nodes or submucosal tissue

734
Q

peripheral tolerance is induced in

A

mature self-reactive lymphocytes

735
Q

central tolerance results in

A

deletion by apoptosis, change of BCR specificity, development of Treg cells

736
Q

peripheral tolerance results in

A

induction of anergy, deletion by apoptosis, suppression by Treg cells

737
Q

positive selection deletes by apoptosis what kind of cells

A

no affinity towards self-Ag

738
Q

negative selection deletes by apoptosis what kind of cells

A

strong affinity towards self-Ag

739
Q

natural Treg cells are generated in the

A

thymus

740
Q

what other cells can develop Treg phenotype outside the thymus

A

mature Th0 cells, differentiate into induced Treg (iTreg) cells

741
Q

FOXP3 expression can be induced in naïve CD4 cells in vitro upon Ag recognition in the presence of

A

TGFb

742
Q

naïve CD4 T cell + TGFb + IL-6 + retinoic acid

A

induces expression of RAR and RORgt leading to development of Th17 cell

743
Q

naïve CD4 T cell + TGFb + IL-2

A

induces expression of FOXP3 leading to expression of iTreg

744
Q

iTreg cells are produced in the

A

lymph nodes (LNs) and GI tract

745
Q

TGFb, IL-10, IL-4 from Treg cells downregulates what in APCs

A

CD40, B7, IL-12

746
Q

TGFb, IL-10, IL-4 from Treg cells increases expression of what in APCs

A

IL-10

747
Q

cell with inadequate B7:CD28 costimulation undergoes

A

induction of anergy

748
Q

anti-CTLA-4 and anti-PD-1 therapy enhances

A

antitumor immune response and tumor regression (inhibits suppression of T cell response)

749
Q

T cell deletion by apoptosis occurs by what two pathways

A

mitochondrial (intrinsic), death receptor (extrinsic)

750
Q

T cell deletion by apoptosis: mitochondrial (intrinsic) pathway involves

A

Bax, Bak, cytochrome c, caspase 9

751
Q

T cell deletion by apoptosis: death receptor (extrinsic) pathway involves

A

Fas:FasL(T cell), TNF:TNFR(T cell), caspase 8

752
Q

preB cells express what type of chain

A

rearranged Ig H chain

753
Q

all B cells that contain what kind of chain underwent BCR editing

A

lambda Ig L chain

754
Q

inhibitory receptor of B cell

A

CD22

755
Q

role of CD22

A

attenuate BCR signaling

756
Q

mechanism of CD22 attenuation of BCR signaling

A

phosphorylated by Lyn, recruits SHP-1 tyrosine phosphatase

757
Q

commensal microbes

A

reside in intestinal and respiratory tracts and on the skin

758
Q

anti-inflammatory activity of normal microflora mediated by

A

Treg and IL-10

759
Q

GALT

A

gut associated lymphoid tissue

760
Q

two broad mechanisms of autoimmunity

A

susceptibility genes and environmental triggers

761
Q

AIRE gene expressed in

A

medullary thymic epithelial cells

762
Q

AIRE genes responsible for

A

production of tissue restricted Ags (TRAs) used in central tolerance

763
Q

AIRE deficiency results in

A

breakdown of T cell negative selection (cannot delete self-reactive T cells)

764
Q

CR1 located

A

RBC

765
Q

CR1 on RBCs binds

A

C3b of ICs

766
Q

in spleen and liver, macrophages remove ICs from RBCs through interaction of

A

CR1:C3b and FcR:Fc (stronger synapse)

767
Q

CTLA-4 KO mice have what problems

A

uncontrolled lymphocyte activation (massive LNs) and fatal multi-system lymphocytic infiltrates

768
Q

CTLA-4 deficiency associated with

A

type I diabetes mellitus and Grave’s disease

769
Q

cell-intrinsic function of CTLA-4

A

block signal of APC to inhibit T cell activation

770
Q

cell-extrinsic action of CTLA-4

A

reduced B7 costimulation of T cell to inhibit T cell activation

771
Q

Treg + APC + CTLA-4:B7 + CD28:B7

A

cell-intrinsic T cell inhibition by CTLA-4

772
Q

Treg + APC + CTLA-4:B7

A

cell-extrinsic T cell inhibition by CTLA-4

773
Q

four ways autoimmunity is prevented

A

tolerance, deletion, inhibition, suppression

774
Q

prevention of autoimmunity: tolerance

A

specific Ag (e.g BBB) cannot become activated

775
Q

prevention of autoimmunity: deletion

A

T cell that express Fas/CD95 can receive signals from FasL and undergo apoptosis

776
Q

prevention of autoimmunity: inhibition

A

CTLA-4/CD152 binds B7/CD80 on APC and inhibits costimulatory signal

777
Q

prevention of autoimmunity: suppression

A

Treg inhibits through production of IL-10 and TGFb

778
Q

examples of immune privileged sites

A

eye, brain, pregnant uterus, ovary, testis, adrenal cortex, hair follicles

779
Q

most of autoimmune disease associated with what HLA

A

HLA-II

780
Q

three ways environment results in autoimmunity

A

molecular mimicry, polyclonal (bystander) activation, release of previously sequestered Ag (DAMPs)

781
Q

type I (immediate) hypersensitivity

A

mediated by IgE, results from actions of mast cell mediators

782
Q

type II hypersensitivity

A

mediated Ab self-reacting with normal tissue, results from action of complement

783
Q

type III hypersensitivity

A

mediated by circulating ICs that deposit in vessels, results from action of complement

784
Q

type IV (delayed) hypersensitivity

A

mediated by T cells, results from action of inflammatory cytokines or killing of host cells

785
Q

type I most often triggered by

A

environmental Ags

786
Q

atopic disease

A

allergies

787
Q

mast cell mediators: histamine

A

dilation of small vessels, vascular permeability

788
Q

mast cell mediators: proteases

A

local tissue damage

789
Q

mast cell mediators: prostaglandins

A

vascular dilation

790
Q

mast cell mediators: leukotrienes

A

prolonged smooth muscle contraction

791
Q

mast cell mediators: cytokines

A

induce local inflammation

792
Q

why second exposure to allergen is more severe than first during type I hypersensitivity

A

plasma cells make IgE to allergen, IgE bound by RcRe/CD23 on mast cells

793
Q

late-phase (2-24 hours after secondary exposure to allergen) mast cell response characterized by

A

inflammatory infiltrate rich in eosinophils, neutrophils, and T cells

794
Q

asthma

A

local type I hypersensitivity reaction

795
Q

asthma is the reversible bronchiole lumen obstruction caused by

A

action of mast that stimulate local airway inflammation and bronchospasm

796
Q

anaphylaxis

A

systemic type I hypersensitivity reaction

797
Q

positive allergen testing

A

redness and swelling within 20 to 30 minutes of exposure

798
Q

allergen-specific immunotherapy (allergen-SIT)

A

only curative approach to allergic disease, administration of increasing doses of allergen

799
Q

allergen-SIT

A

increase threshold for mast cell activation, generation of iTreg cells, production of greater proportion of IgG to distract allergen from IgE

800
Q

type II hypersensitivity: IgG and IgM activate CP, resulting in

A

production of C3a and C5a for inflammation and neutrophil chemotaxis

801
Q

type II hypersensitivity: phagocytosis induced by

A

FcRg or CR1 receptors on macrophages

802
Q

type II hypersensitivity: ADCC induced by

A

FcRgIII on NK cells

803
Q

Grave’s disease

A

type II hypersensitivity, stimulate thyroid activity by Abs specific for TSH receptor, hyperthyroidism

804
Q

Myasthenia gravis

A

type II hypersensitivity, inhibit acetylcholine signaling by Abs specific for AChR, muscle weakness and paralysis

805
Q

hemolytic disease of the newborn: mother and fetus Rh phenotypes

A

related to type II hypersensitivity, mother Rh-negative, fetus Rh-positive

806
Q

drug-induced immune hemolytic anemias (DIIHA)

A

related to type II hypersensitivity

807
Q

DIIHA: penicillin-induced

A

hapten model, drug binds directly to RBC surface, hemolysis by complement or phagocytosis

808
Q

DIIHA: quinidine-induced

A

IC formation model, ICs bind RBC surface through CR1, hemolysis by complement

809
Q

DIIHA: methyldopa-induced

A

autoimmune model, methyldopa Ab cross-reacts with Rh Ag on RBC surface, hemolysis by phagocytosis

810
Q

autoimmune hemolytic anemia

A

type II hypersensitivity, Rh and I blood group Ags on RBC surface, hemolysis by phagocytosis, anemia

811
Q

autoimmune (idiopathic) thrombocytopenic purpura

A

type II hypersensitivity, gpIIb/IIIa integrin on RBC surface, hemolysis by phagocytosis, bleeding

812
Q

Goodpasture’s syndrome

A

type II hypersensitivity, complement targets non-collagenous basement membrane proteins of kidney glomeruli and lung, nephritis and lung hemorrhage

813
Q

pemphigus vulgaris

A

type II hypersensitivity, epidermal cadherin, activation of proteases, skin vesicles (bullae)

814
Q

pernicious anemia

A

type II hypersensitivity, gastric intrinsic factor, decreased absorption of B12

815
Q

rheumatic fever

A

type II hypersensitivity, Abs produced against Streptococcal cell wall cross react with myosin, myocarditis and arthritis

816
Q

systemic lupus erythematosus (SLE)

A

type III hypersensitivity, DNA and nucleoproteins, nephritis, arthritis, vasculitis

817
Q

polyarteritis nodosa

A

type III hypersensitivity, often microbial Ags, vasculitis

818
Q

post-streptococcal glomuronephritis

A

type III hypersensitivity, streptococcal cell wall Ag, nephritis

819
Q

serum sickness (clinical and experimental)

A

type III hypersensitivity, various protein Ags, systemic vasculitis, nephritis, arthritis

820
Q

arthus reaction (experimental)

A

type III hypersensitivity, SQ administration of protein Ag to previously immunized animal, local cutaneous vasculitis

821
Q

how tissue injury occurs during type IV hypersensitivity

A

CD4 (Th1 and Th17) mediated inflammation, CD8 CTL mediated host cell killing

822
Q

most important microbial trigger of type IV hypersensitivity

A

Mycobacterium tuberculosis

823
Q

delayed type hypersensitivity (DTH)

A

type IV hypersensitivity related, mainly CD4 T cell mediated, develops 24-48 hours after Ag exposure

824
Q

how humans may become sensitized to DTH reactions

A

previous TB infection or contact sensitization

825
Q

purified protein derivative (PPD)

A

protein Ag of Mycobacterium tuberculosis used in DTH testing

826
Q

allergic contact dermatitis (ACD)

A

type IV hypersensitivity related, results from DTH reactions

827
Q

most common cause of ACD

A

metals (nickel and cobalt in costume jewelry, chromium in leather)

828
Q

multiple sclerosis (MS)

A

type IV hypersensitivity, myelin proteins, sensory and motor dysfunction

829
Q

rheumatoid arthritis (RA)

A

type IV hypersensitivity, unknown Ags in join, inflammation of synovium, erosion of cartilage and bone

830
Q

type 1 diabetes mellitus (type I DM)

A

type IV hypersensitivity, pancreatic islet Ags, impaired glucose metabolism, vascular disease

831
Q

inflammatory bowel disease (IBD, Chron’s disease)

A

type IV hypersensitivity with microbial component, aberrant reaction to intestinal microflora, bowel wall inflammation, diarrhea, hemorrhage

832
Q

contact sensitivity (poison ivy)

A

type IV hypersensitivity, modified skin proteins, DTH reaction in skin

833
Q

chronic infection (TB)

A

type IV hypersensitivity with microbial component, chronic granulomatous inflammation

SFM Immunology (1 decks)

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