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Block 6: Immunology and Inflammation > Week 1 > Flashcards

Week 1 Flashcards

1
Q

eosinophil

A

kills ab-coated parasites through release of granule contents

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2
Q

basophil

A

controls immune response to parasites

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3
Q

megakaryocyte

A

make platelets, repair wounds

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4
Q

erythrocyte

A

oxygen transport

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5
Q

small lymphocyte (B)

A

make antibodies

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6
Q

small lymphocyte (T)

A

make cytotixc and helper functions

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7
Q

dendritic cells

A

activate t cell and initiate ADAPTIVE immune responses

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8
Q

plasma cell

A

fully differentiated form of B cell that secretes antibodies

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9
Q

mast cell

A

expulsion of parasite from body through release of granules containing histamine and other active agents

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10
Q

NK cell

A

kill cells infected with certain viruses

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11
Q

monocyte

A

precursor to macrophage

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12
Q

neutrophil

A

phagocytosis and killing of microorganisms

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13
Q

macrophage

A

phagocytosis and killing microorganisms
activate T cells
initiate immune responses

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14
Q

primary lymphoid organ

A

bone marrow and thymus

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15
Q

bone marrow

A

essential for B cell development and all cells mediating innate immunity

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16
Q

thymus

A

essential for T cell development

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17
Q

secondary lymphoid tissues

A

spleen, gut (payer’s patch) , lymph node

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18
Q

combinatory diversity

A

heavy chain, kappa light chain and lambda light chain each have a certain amount of combinations that can occur

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19
Q

RAG1 and Rag2

A

recognize and cleave unique recombination signals sequences that flank immunoglobulin gene segments

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20
Q

VDJ recombinase

A

enzyme that mediates rearrangements of immunoglobulin gene rearrangement and T cell receptor gene rearrangment

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21
Q

what causes SCID?

A

severe combined immunodeficiency; genetic deficiency in either RAG 1 or RAG2 causes complete absence of lymphocytes

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22
Q

terminal deoxynucleotidyl trnasferase

A

TdT can add extra nucleotides

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23
Q

junctional flexibility

A

mechanism of diversity that can add/subtract nucleotides at junction; changes coding sequences and INCR ab diversity

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24
Q

allelic exclusion

A

a given b cell has a single functional heavy chain and a single functional light chiain –> can produce ONE type of antibody with a SINGLE antigenic specificity

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25
Q

what do B cells that are coming out of the bone marrow have on their surface

A

IgM and IgD

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26
Q

How is it possible that a B cell can express IgM and IgD at the same time

A

RNA splicing

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27
Q

RNA splicing

A

allows for antibody molecule to be expressed in transmembrane or secreted form

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28
Q

lag period

A

4-7 days after infection begins during which time the body is mounting primary immune response

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29
Q

what immunoglobulin is predominant during primary response

A

IgM

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30
Q

what immunoglobulin is predominant during secondary response

A

IgG

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31
Q

is the primary response dependent on T cells?

A

no, the primary response is both thymus dependent and thymus independent (you don’t need t cells for primary response)

note that the secondary response IS T cell dependent

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32
Q

what is the lag period for the secondary response

A

1-3 days

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33
Q

why are somatic mutations important in gene regions coding for antibodies?

A

somatic mutations in the variable region accumulate to allow for the affinity of the antibody to increase for the antigen

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34
Q

affinity maturation

A

random mutations that can increase or decrease ab affinity for antigen; can also be neutral

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35
Q

what occurs in the germinal center?

A

somatic hypermutations, class switch recombination, devel of plasma and mem b cells

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36
Q

class switching and mutation depend on…

A

antigen and T cell; in secondary lymphoid organs

DO NOT DEPEND ON RAG

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37
Q

AID

A

lymphocyte specific enzyme required for class switching and somatic mutation

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38
Q

what are the mechanisms required for variable region diversity

A 
gremline segments (V,D,J) 
combinatorial joining
juncitonal diversity 
association of diverse heavy and light chains
somatic mutations
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39
Q

what region does class switch affect?

A

heavy chain constant region

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40
Q

CD molecules associated with B cell lineages

A

CD19, CD20, CD10

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41
Q

opsonization

A

antibody bound to bacteria enhances their phagocytosis

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42
Q

phagolysosome

A

lysosomes fused with phagosomes ( the lysosomes provide the enzymes that degrade the bacteria)

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43
Q

what do Fc receptors on neutrophils and macrophages bind to?

A

IgG bound to antigen –> opsonization

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44
Q

systemic lupus erytheamtosus

A

DNA:anti-DNA antibodies
kidney failure
Ag:Ab mediated immunopathology

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45
Q

RhoD immune globulin to Rh factor

A

prevents Rh based hemolytic disease of newborns

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46
Q

Humira (and Embrel)

A

monoclonal antibodies to TNFalpha (which mediates pathology in arthritis

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47
Q

Tysabri

A

monoclonal Ab that blocks adhesion molecules on T cells –> prevent ability to go to brain/GI

chrone’s disease and MS

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48
Q

polyclonal ab response

A

most microbes express many different antigens; ab secreted by dif b cell lineages

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49
Q

Hemagglutination

A

used for typing red blood cells. Antisera specific for the A or B antigens on red blood cells are used as reagents to detect the type of antigen present.

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50
Q

how many binding sites on each IgG

A

2 antigen combining site; capacity for cross linking

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51
Q

what forces mediate antigen-antibody interactions?

A

hydrogen bonding
ionic bonding
van der waals (hydrophobic interactions)

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52
Q

hapten

A

a molecule with only a single epitope

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53
Q

law of mass action

A

antigen antibody reactions are reversible; equilibrium constant or affinity = “K”

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54
Q

affinity

A

strength of a single antigen combining site of an antibody and a single epitope on an antigen

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55
Q

avidity

A

strength of binding of antibody for an antigen

multivalent antigens bind with greater avidity because the antibody can bind two epitopes, not just one

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56
Q

which has greater avidity- IgM or IgG

A

IgM because it has more binding sites

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57
Q

post streptococcal pharyngitis

A

10% untreated get rheumatic fever –> immune damage to cardiac valves –> because the streptocococcal ag cross react with cardiac tissue

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58
Q

benefits of cross reacting antigens

A

vaccines (use molecules that are similar but not the same to the toxin)

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59
Q

what determines how much visible preccip forms

A

size of complexes –> depends on amount of cross linking

need complex to get big to fall out of precipitate

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60
Q

when does maximal precipitation occur

A

equivalence; ag/ab is in slight antigen excess

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61
Q

agglutination

A

combination of an antibody with a particulate antigen

resulting in visible clumps that form within minutes

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62
Q

particulate antigen

A

RBC, latex, bacteria

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63
Q

titer

A

1/highest dilution of antiserum that still gives positive agglutination reaction

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64
Q

precipitin reaction

A

combination of an antibody with a SOLUBLE antigen (protein, polysaccharide) forming a lattice that, if it gets big enough, can fall out of solution and form visible precipitate

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65
Q

radioimmunoassay

A

inhibition assay

66
Q

ELISA (EIA)

A

enzyme linked immunosorbent assay allowing you to measure antibody in serum

67
Q

indirect fluorescence

A

looking for antibodies in patients serum; add FI-labeled anti-Ig

68
Q

direct fluoresnces

A

identify T cells in periphery; add FI-labeled antibody

69
Q

flow cytometry

A

automated analysis of cell subsets in a mix

70
Q

envelope of a virus

A

derived from host; contains viral glycoprotein

71
Q

capsid

A

coat; protein shell surrounding nucleic acid genome

72
Q

nucleocapsid

A

core; nucleic acid-protein assembly packaged within the viron

73
Q

virion

A

infection virus particle

74
Q

tegument

A

structure containing regulatory proteins; include transcription and translation factors;

75
Q

where is the tegument located

A

between nucleocapsids and envelope

76
Q

what kind of virus is influenza

A

RNA enveloped

77
Q

what kind of virus is Hep A

A

RNA nucleocapsid

78
Q

what kind of virus is poliovirus

A

RNA nucleocapsid

79
Q

what kind of virus is herpes

A

DNA enveloped virus

80
Q

what kind of virus is Hep B

A

DNA enveloped virus

81
Q

what kind of virus is epstein barr

A

DNA enveloped virus

82
Q

+ polarity

A

RNA with the same base sequence as the mRNA

83
Q
  • polarity
A

RNA sequence that is complimentary to the mRNA

84
Q

segmented

A

several fragments of RNA that make a complete virus genome

85
Q

reassortment

A

exchanging entire RNA molecules between “genetically related” viruses w/ segmented genomes

86
Q

recombination

A

exchanging nucleotides seq among dif RNA molecules

87
Q

proteins on the surface of HIV

A

GP41 and GP120

88
Q

proteins on the surface of flu

A

hemagluttinin and neuraminidase

89
Q

cxcr4

A

7 transmembrane protein on surface of T cell; binds Gp41 and GP120 of HIV virus

90
Q

CD14

A

binds LPS/LPSBP

91
Q

HMGB1

A

histone protein secreted by macrophages during inflammation

92
Q

what kind of peptidoglycan layer does gram neg bacteria have

A

very thin

93
Q

TLR2

A

peptidoglycan
lipoproteins

gram positive bacteria!!! (also yeast)

94
Q

TLR4

A

LPS, F-protein

gram negative bacteria (also RSV)

95
Q

RSV

A

respiratory syncytial virus; recognized by TLR4
uncaring occurs at cell membrane
RNA enveloped virus

96
Q

IL1

A

Fever; Activates endothelial cells

97
Q

IL 12

A

Activates NK cells

98
Q

TNF alpha

A

Causes tissue damage and mediates septic shock

99
Q

IL 6

A

Induces acute phase proteins in the liver

100
Q

IL8

A

chemotactic for PMNs (neutrophils)

101
Q

HMGB1

A

A late mediator of sepsis (a histone protein)

secreted by macrophages during inflammation

102
Q

serovar

A

subspecies classification based on a distinct antigenic variant of a species

103
Q

criteria for confounder

A
  1. risk factor for disease in unexposed group
  2. associated with the exposure
  3. not in causal pathway
104
Q

what is a confounder?

A

it is a factor on which the exposed and unexposed differ that can cause mixing of effect

105
Q

types of misclassification

A

non-differential and differential

106
Q

types of bias

A

information and selection

107
Q

describe types of info bias

A

diagnostic bias, recall bias, interview bias

108
Q

describe types of selection bias

A

inclusion/exclusion, group bias, surveillance patterns, non-response rate

109
Q

how to handle confounding

A
  1. Restriction
  2. Matching
  3. Randomized
  4. Analysis (stratified or multivariate)
110
Q

what kind of Fc do mast cells and basophils have

A

Fc for IgE

111
Q

what kind of Fc do neutrophils and macrophages have

A

Fc for IgG

112
Q

what are the two most sensitive lab techniques?

A

ELISA and Radioimmunoassay

113
Q

cross reacting antigens

A

based on ab:ag cleft, more than one ag may be able to bind an ab; this is why vaccines work and also why rheumatic fever develops

114
Q

how can B cell simultaneously express both IgM and IgD?

A

RNA splicing; note that a B cell emerging from bone marrow will express both IgM and IgD on surface

115
Q

how can an antibody molecule be expressed in transmembrane or secreted form?

A

RNA splicing

116
Q

what are the key events of B cell development in the germinal center?

A

somatic hypermutaiotn and class switch

note - requires T cell and antigen

117
Q

where do DNA viruses replicate?

A

nucleus with the exception of poxvirus which replicates in the cytoplasm

118
Q

Where do RNA viruses replicate?

A

cytoplasm with the exception of flu which replicates in nuclear

119
Q

RNA dependent RNA pol

A

used by ALL RNA viruses except retroviruses, which use a RNA dependent DNA polymerase

120
Q

infectious nucleic acid

A

viruses that do not require polymerase in the vision

121
Q

ways to make mRNA and viral proteins

A

post translational cleavage
splicing
multi subgeneric RNAs

122
Q

what viruses use post translational cleavage

A

HIV , polio , HTLV

123
Q

which viruses use splicing

A

HIV< HTLV, flu HBV, AAV, adenovirus

124
Q

which viruses use multiple subgeneric mRNAs

A

adenovirus, herpes, pox

125
Q

three mechanisms for origin of diversity of RNA virus genomes

A

misincorporation of nucleotides
segment reassortment/recomb
editing

126
Q

defensins

A

small MW proteins w/ antibiotic properties

found in neutrophils

127
Q

cationic proteins

A

largeMW, in lysosomes of neutrophils, punch holes in microbial membranes

128
Q

lysozyme

A

enzyme breaks down peptidoglycan cell wall

129
Q

myeloperoxidase

A

enzyme only in neutrophils that converts H2O2 to hypochlorites

130
Q

where are reactive nitrogen species found

A

only in macrophages

131
Q

acute phase response proteins

A

C reactive protein
mannose binding lectin
LPS-BP
serum amyloid P

132
Q

what can trigger TLR?

A 
dsRNA
CpGs (unmethylated) 
bacterial flagella
LPS 
peptidoglycan of gram+
133
Q

examples of DAMPs

A 
heat shock proteins
urate crystals (gout) 
HMGB1 = marker of cell damage
134
Q

TLR5

A

recognizes flagellin

135
Q

IL8

A

chemotactic for neutrophils

136
Q

cytokine storm

A

massive ants of TNF alpha IL1 IL6 and IL12 to mobilize phagocytes; can cause septic shock and multiple organ dysfunction

137
Q

what role does nitric oxide have in septic shock?

A

activated macrophages induce iNOS, contribute to lowering BP

138
Q

relationship between IL1 and IL6

A

IL1 induces production of IL6

139
Q

low conc of TNF

A

local inflammation, upreg of adhesion molecules, IL1 and chemokines

140
Q

moderate TNF

A

fever, acute phase proteins, mobilize leukocytes from bone marrow

141
Q

high quantities of TNF

A

septic shock

142
Q

what are the endpoints of complement

A

inflammation
microbicidal activity
increased phagocytosis
opsonizaiton

143
Q

what initiates the classical pathway of complement

A

ag-ab complex

144
Q

what system is mannose binding lectin a part of

A

innate immunity; recognizes microbes in absence of antibody; it is a protein in the serum that can bind the carbohydrate mannose, which is found on the surface of many microbes

145
Q

CRP

A

part of the innate immune system bc does not require antigen, but it triggers the CLASSICAL pathway

146
Q

hereditary angioneurotic edema

A

absence of C1 esterase inhibitor, which usually blocks C1r and C1s
therefore, patients have often triggering of complement

147
Q

what are the plasma protein regulators of complement

A

Factors H and I
C1 esterase inhibitor
Carboxypeptidases (degrade the anaphylaxins)

148
Q

regulators of complement

A

plasma proteins
short half life of many components
membrane bound proteins

149
Q

what are the membrane bound protein regulators of complement

A

DAF
MCP
HRF

150
Q

paroxysmal nocturnal hemoglobulinuria

A

defect in homologous restriction factor and CD59, which both block MAC and interfere with C9 polymerization; therefore, you don’t have the anchor for factors and RBCs lyse –> clinical sign is waking up with dark pee

151
Q

DAF

A

delay accelerating factor that breaks down C4b2a and C3bBb

152
Q

MCP

A

membrane cofactor protein that dissociates C4b2a and C3bBb and facilitates C4b and C3b degradation by factor I

153
Q

factor I deficiency

A

uncontrolled activation of alternate pathway and depletion of C3

154
Q

deficiency in C5-C8, factor D , properdin

A

susceptibility to gram negative infections, esp neisseria

155
Q

what immunoglobulin for parasites

A

IgE

156
Q

cell types doing ADCC

A

NK, neutrophils, eosinophils and macrophages and monocytes

157
Q

segmented filamentous bacteria

A

causes up regulation of TH17 secreting cells

158
Q

bacteria assoc with healthy micro biome?

A

bacteriodetes and bifidobacterium

159
Q

bacteria NOT assoc w healthy micro biome?

A

proteobacteria and clostridia

160
Q

CD25+ cells

A

treg (also FoxP3+)

Block 6: Immunology and Inflammation (6 decks)

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