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Immunology > Block 2 > Flashcards

Block 2 Flashcards

1
Q

IL-__ and IL-__ lead to T cells

A

2
7

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2
Q

IL-__ leads to B cells

A

4

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3
Q

do B or T cells perform somatic mutation during generation of antibody binding diversity

A

B

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4
Q

is VDJ associated with light or heavy chain of an antibody

A

heavy

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5
Q

is VJ associated with light or heavy chain of an antibody

A

light

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6
Q

what is junctional diversity during antibody generation

A

nucleotides are added or deleted during V(D)J recombination by Tdt enzyme to produce hypervariable regions

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7
Q

what is somatic hypermutation

A

mutations in V genes of heavy or light chains in the germinal center for B cells, with the goal to produce high affinity antibodies
*B cells only, occurs in dark zone of germinal center

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8
Q

what 3 enzymes are needed for
V(D) J recombination

A

RAG-1
RAG-2
TdT

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9
Q

what is the main V(D)J recombination gene

A

RAG

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10
Q

what happens if there is a decrease in TdT for V(D)J recombination

A

decrease in antibody diversity

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11
Q

what is another name for hypervariable region

A

complementarity determining region

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12
Q

what is the result of agammaglobinulinemia

A

inability to make antibodies

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13
Q

with x linked mutation causing agammaglobinemia, what gene is mutated

A

BTK

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14
Q

where is the first checkpoint in B cell receptor development

A

between pre-BCR and immature B

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15
Q

what gene segment do light chains of antibodies not have

A

D

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16
Q

what is receptor editing during B cell receptor development

A

if the rearranged kappa chain fails to bind, try the kappa on the chromosome from the other parent
if recombination still fails, it is tried `on the lambda chain

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17
Q

at the immature B cell level, if the receptor binds, signals are delivered that promote survival and there is a shutdown of what gene activity

A

RAG

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18
Q

when B cells just come out of bone marrow, they express both Ig__ and Ig__

A

M
D

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19
Q

where does isotype switch occur

A

germinal center light zone

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20
Q

what is the difference in structure between membrane bound Ig and secreted Ig

A

membrane bound has a hydrophobic tail that anchors it to the membrane

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21
Q

what enzyme associated with CD4 and CD8 mediates phosphorylation to transmit a signal

A

LCK

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22
Q

the alpha chain of T cells is similar to the __ chain of B cells, as they both are involved in VJ recombination

A

light

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23
Q

the complementarity determining region (hypervariable region) of a TCR variable region interacts with __ of an MHC molecule

A

peptide

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24
Q

in T cells, VDJ recombination occurs between __ and __

A

double - —> double +

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25
Q

weak recognition of MHC by T cells is positive or negative selection

A

positive

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26
Q

strong recognition of MHC by T cells is positive or negative selection

A

negative

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27
Q

what is Omenn syndrome caused by

A

RAG mutation= messed up T cells, no B cells
*diversity of proteins on the surface of B cells and T cells is severely limited, impairing the cells’ ability to recognize foreign invaders and fight infections

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28
Q

what is the question asked with T cell positive selection

A

will the cell become CD4+ or CD8+

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29
Q

what is the question asked with T cell negative selection

A

does the cell react with self
yes (strong recognition of MHC)= apoptosis

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30
Q

what is the difference between alphabeta and gammadelta T cells

A

gammadelta don’t go through selection so they aren’t as restricted
*still go through VDJ recombination

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31
Q

what are the 3 functions of gammadelta T cells

A

cytokine/chemokine production
dendritic cell maturation
antigen presenting

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32
Q

what accounts for no B or T cell recognizing the same antigen

A

variability in V region at hypervariable region (complementarity determining region)

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33
Q

cellular immunity is mediated by what cells

A

T cells

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34
Q

what are 2 ways in which naive T cells can enter a draining lymph node

A

blood
afferent lymph from an upstream lymph node

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35
Q

what does expression of CCR7 on dendritic cells or T cells means

A

can be trafficked to lymph node paracortical region

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36
Q

what are the 3 steps to T cell activation

A
  1. antigen presentation on class I or II MHC at antigen presenting cell surface
  2. co-stimulation (1 molecule on antigen presenting cell interacts with one molecule on T cell)
  3. production of cytokines
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37
Q

what is the co-stimulation molecule on naive T cells during T cell activation

A

CD28

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38
Q

what are the 2 possible co-stimulation molecule present on antigen presenting cells during T cell activation

A

CD80/86
B7.1/B7.2

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39
Q

what is the importance of Zap-70 in antigen recognition

A

it’s needed to get a T cell response to T cell stimulation

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40
Q

what is the effect of no Zap-70 in antigen recognition

A

abnormal T cell receptors result in low to normal CD4, and low CD8
T cells don’t respond to T cell stimulation, resulting in repeated viral infection due to lack of mature T cells

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41
Q

what is the function of the immune synapse

A

to activate protein kinase C for T cell response

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42
Q

an influx in what ion occurs during T cell activation

A

calcium

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43
Q

what is the result of calcium release activated channels deficiency in T cell activation

A

immunodeficiency due to limited T cell activation

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44
Q

for co-stimulation for T cell activation, what is the signal present on the antigen presenting cell

A

B7.1/B7.2 (CD80/CD86)

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45
Q

for co-stimulation for T cell activation, what is the signal present on the naive T cell

A

CD28

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46
Q

what does the presence of CD40L on T cells indicate

A

the T cell is an effector T cell which can boost macrophage killing or induce class switch on T cells

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47
Q

what is IL-2 secretion needed for

A

T cell proliferation

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48
Q

what is clonal expansion in T cells

A

increase then contraction of T cells in response to the number of days since infection and T cell activation

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49
Q

non-classical antigen presentation involves what 2 types of molecules

A

lipids
glycolipids

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50
Q

what is non-classical antigen presentation

A

CD1 is a surface glycoprotein that can present lipids/glycolipids to T cells instead of peptides

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51
Q

what T cells do CD1 glycoproteins express their glycolipid/lipid to

A

alphabeta T cells
gammadelta T cells
NKT cells

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52
Q

what type of cells are NKT cells

A

antigen presenting

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53
Q

what does it mean to say NKT cells are semi-variant

A

they only have one Valpha and limited Vbeta genes

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54
Q

NKT cells only bind with __

A

CD1d

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55
Q

NKT cells only bind with __

A

CD1d (recognize glycolipids and lipids)

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56
Q

how is the binding of a superantigen different than that of an antigen

A

the superantigen binds to the side of the MHC class II and beta chain of CD4+T cell leading to non-specific T cell activation and an increased immune response

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57
Q

what are the 4 types of effector T cells naive CD4+ T cells can become

A

Th1
Th2
Th17
Tfh (follicular helper)

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58
Q

what are the 3 possible roles of effector T cells

A

help B cells proliferate/differentiate to plasma cells
help promote innate activity (make macrophages kill more)
help T cells proliferate/differentiate to effector CD8+ cells

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59
Q

what 2 cytokines are released in response to large intracellular microbes

A

IL-12
IFNgamma

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60
Q

what class of T helper cells clear intracellular larger microbes

A

Th1

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61
Q

what cytokine is released in response to a helminths (worm) infection

A

IL-4

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62
Q

what class of T helper cells clears worm infections

A

Th2

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63
Q

what cytokines are released in response to extracellular fungi and bacteria (smaller stuff)

A

IL-1
IL-6
TGF-beta
IL-23

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64
Q

what class of T helper cells clears extracellular fungi and bacteria

A

Th17

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65
Q

what is the main cytokine that signals Th17 pathway

A

IL-23

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66
Q

what 3 cells do Th1 cells activate

A

macrophages
killer T cells
B cells

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67
Q

what 4 cells do Th2 cells activate

A

eosinophils
mast cells
basophils
macrophages (M2)

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68
Q

what cell does Th17 recruit

A

neutrophils

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69
Q

what 3 cytokines do Th1 cells secrete

A

IFN-gamma
TNF-alpha
IL-2

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70
Q

what 3 cytokines do Th2 cells secrete

A

IL-4
IL-5
IL-13

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71
Q

what is the function of IL-17 release from Th17 cells

A

increase neutrophil response
push inflammatory response
improve epithelial cells

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72
Q

Th23+IL-6+IL-1+TGF-beta–>Th__
–>continued __ response

A

17
inflammatory

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73
Q

what STAT protein is needed for Th17 response

A

STAT3

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74
Q

what is involved in hyper IgE syndrome

A

loss of STAT so no Th17= increased susceptibility to bacterial and fungal infections

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75
Q

CD8+ killer T cells are upregulated by Th__ activity

A

1

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76
Q

how does perforin/granzyme mediated cell killing work

A

target cell and CD8+ T cell interact and form a synapse
CD8+ cell releases perforin granules into synapse
uptake of perforin and granzyme into target cell cytosol, creating an endosome
perforin pokes hole in endosome and granzymes flow out into cell, activating caspase and apoptosis in target cell

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77
Q

how does Fas/Fas-L mediated cell killing work

A

Fas-L on CD8+ T cell interacts with Fas on target cell, triggering caspase activity and apoptosis of target cell

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78
Q

how can CD4+ T cells provide help to CD8+ T cells

A

CD4+ T cells secrete IFN-gamma, increasing activity of CD8+

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79
Q

once T cells are effector cells, how do they get to their destination

A

effector T cells upregulate different selectins/integrins depending on where they go to

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80
Q

what 2 cytokines are requires for memory T cell development

A

IL-7
IL-15

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81
Q

what is the difference between central and effector memory T cells

A

central- stay in lymph node
effector- localize where they encounter the antigen so will be quick to respond to future antigen at same site

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82
Q

what is familial hemophagocytic lymphohistiocytosis

A

out of control macrophages secreting a lot of cytokines and eating everything due to a defect in lymphocyte cytotoxicity

83
Q

where are marginal zone B cells located

A

peripheral region of splenic white pulp

84
Q

most B cells are called __ because they reside in and circulate through the follicles of lymphoid organs

A

follicular

85
Q

for T dependent responses, what 3 steps are required

A

activation of T cell
activation of B cell
2 interaction of B and T cells (1 interaction to proliferate, 1 signal to class-switch)

86
Q

where does the first interaction between T and B cells occur in T dependent B cell activation

A

outside the lymph follicle

87
Q

what is involved in the first interaction between B and T cells for thymus dependent antigen response

A

T cell instructs B cell to proliferate in dark zone and perform somatic hypermutation to increase binding affinity

88
Q

what protein is required for somatic hypermutation

A

AID

89
Q

what is involved in the second interaction between B and T cells for thymus dependent antigen response

A

B cell with best BCR interacts with T follicular helper cells (ICOS on T cell interacts with ICOS-L on B cell) and follicular dendritic cells (CD40 on B cell interacts with CD40-L on T cell) that instruct B cell to class switch in light zone

90
Q

thymus independent antigens are what type of molecules

A

polysaccharides

91
Q

do thymus independent or dependent antigens perform class switching

A

dependent

92
Q

do thymus independent or dependent antigens have high affinity

A

thymus dependent

93
Q

do thymus independent or dependent antigens produce memory B cells

A

thymus dependent

94
Q

thymus independent-1 antigens make IgM antibodies through use of what 3 stimulations

A

BCR
CD21 (C3d)
TLR

95
Q

how do thymus independent-2 antigens make IgM antibodies

A

stimulating a bunch of B cell receptors at once

96
Q

how can a T cell epitope convert from a thymus independent response to a thymus dependent response

A

conjugate the polysaccharide of the independent response to a carrier

97
Q

what is immunologic tolerance

A

elimination/inactivation of lymphocytes that express high affinity for self

98
Q

what do medullary thymic epithelial cells (MTEC) do

A

develop self antigens under the control of AIRE

99
Q

what causes autoimmune polyendocrinopathy-candidiasis ectodermal dystrophy (APECED)

A

lack of AIRE protein leads to autoreactive T cells with failure of central T tolerance

100
Q

what is anergy

A

the down regulation of receptors on B/T cells so they no longer show high affinity for self, downregulating the immune response to self antigens

101
Q

how does CTLA-4 work as an inhibitory receptor for T cells

A

it competitively binds to CD28 and blocks CD28-B7 interaction to ensure the T cell doesn’t get out of control

102
Q

how does PD-1 work an inhibitory receptor

A

it blocks signaling through the TCR leading to death of the T cell

103
Q

what is the function of regulatory T cells (Tregs)

A

inhibit T cell response

104
Q

what 3 cytokines do T regulatory cells (Tregs) express

A

CD4
CD25
FoxP3

105
Q

what is the main cytokine that is required for survival and function of Treg cells, and determines the number of activated T cells

A

IL-2

106
Q

what causes IPEX syndrome

A

deficiency in FoxP3 leading to no central or periphery Treg response

107
Q

what are 3 types of B cell tolerance

A

receptor editing
deletion
anergy

108
Q

how do the inhibitor receptors for peripheral B cell tolerance, FcgammaRIIb and CD22, act through feedback inhibition

A

if there is already a lot of antibody, they dephosphorylate the B cell, making them inactive

109
Q

what are the 2 main feature that favors tolerance to an antigen

A

antigens without adjuvants
high doses of antigen

110
Q

autoimmunity is caused by an error in __ which is triggered due to an environmental stimulus, leading to a break in __

A

MHC
tolerance

111
Q

what is immunity self-tolerance

A

the ability to recognize self-produced antigens as a nonthreat and respond properly to foreign antigens

112
Q

what is hyper IgM syndrome X linked

A

CD40L signal is messed up so no B cell class switching occurs

113
Q

what is hyper IgM syndrome autosomal recessive

A

CD40 or AID mutation occurs so there is no B cell class switching

114
Q

hypersensitivities start with a __ phase then a __ phase

A

sensitivity
elicitation

115
Q

what are the 4 types of hypersensitivity reactions

A

I- allergy
II- cytotoxicity
III- immune complex formation
IV- delayed

116
Q

type I hypersensitivity involved what type of reactions

A

allergy

117
Q

allergic reactions involve production of Ig__

A

E

118
Q

what is involved in antigen sensitization

A

dendritic cell activates T cell to become Th2
Th2 makes IgE
IgE binds to mast cell and causes degranulation

119
Q

what makes a good allergen

A

repeated exposure to antigen

120
Q

is IgE level higher in plasma or tissue

A

tissue

121
Q

__ cells express IgE of a single specificity
__ and __ bind different IgE molecules specific for different antigens

A

B cells
mast cells and basophils

122
Q

what occurs during a sensitization phase for type I hypersensitivity

A

Th2 cell activated, caused B cell class switch to IgE, IgE binds to mast cell

123
Q

what occurs during elicitation during a type I hypersensitivity

A

antigen protein is crosslinked on IgE on mast cell, causing mast cell degranulation

124
Q

what is one of the pathways activated with mast cell degranulation

A

arachidonic acid

125
Q

what is the purpose of the arachidonic acid pathway in type I hypersensitivity

A

make prostaglandins and leukotrienes

126
Q

for type I hypersensitivity to occur, there must be __, __ exposure of B cells to that antigen presented on the MHC of a Th2 cell

A

recurrent. low-dose

127
Q

the immediate phase of allergen exposure involved release of __, while the late phase involved release of __

A

mast cell degranulation
eosinophils

128
Q

In type I hypersensitivity, a wheal and flare reaction occurs
wheal=__
flare=__

A

swelling
redness

129
Q

during late phase of an allergic reaction, after __ hours there is maximum inflammation before inflammation subsides

A

24

130
Q

in asthma and rhinitis, there is an increase in mucous due to in increase in what cytokine

A

IL-13

131
Q

in bronchial asthma during type I hypersensitivity, there is standard inflammation as well as __

A

spasm contraction of smooth muscle surrounding bronchi

132
Q

in an asthma late response, what happens to the airway

A

remodeling that can lead to scarring due to activity of eosinophils and neutrophils

133
Q

chronic responses to asthma involve the entry of __ and __

A

eosinophils
neutrophils

134
Q

how does extrinsic asthma differ from intrinsic asthma

A

extrinsic- hypersensitivity type I reaction
intrinsic-mast cell degranulation without type I hypersensitivity reaction

135
Q

what causes atopic urticaria

A

IgE response to allergens that enter the skin from outside or travel through circulation, causing an allergic response on the skin

136
Q

what is a more severe version of atopic urticaria

A

atopic dermatitis

137
Q

what is atopic dermititis

A

thickening of the skin following scratching

138
Q

what is the pathway involved in atopic dermatitis

A
  1. Th2 activation and release of IL-4, IL-5, and IL-13
  2. scratching
  3. cytokine release
  4. Th1 activation and macrophage/neutrophil increase
  5. thickening of skin
139
Q

what is the primary way of diagnosing type I hypersensitivity

A

skin test to determine wheal and flare reactions

140
Q

why is the RAST test gradually being replaced

A

it tests IgE in serum but IgE is seen more in tissue than serum

141
Q

what is the cause of a penicillin allergy

A

haptenization (penicillin forms a larger molecule which is recognized by our immune system)

142
Q

why do most people not develop a penicillin allergy

A

most people’s MHC class II will not present the haptenized penicillin to T cells

143
Q

what causes red man syndrome

A

IV infusion of vancomycin that causes degranulation of mast cells but not IgE response

144
Q

how does allergy desensitization work

A

the patient received increases dosage of allergen, increasing IL-10 and serum IgG and decreasing IgE

145
Q

type 2 HSR involves ___, while type 3 HSR involves __

A

antibody binding to protein on the cell
immune complex formation and deposition

146
Q

what antibody is involved in type 2 and 3 HSR

A

IgG

147
Q

what is the difference between warm antibody mediated HSR and cold antibody mediated HSR

A

warm- IgG binds protein antigens at core body temp
cold- IgM binds polysaccharide antigens in peripheral circulation

148
Q

what causes erythroblastosis fetalis

A

Rh- mother is sensitized during birth of first Rh+ child
anti-Rh IgG can cross placenta and bind to Rh antigens of the next Rh+ child RBC
results in lysis of fetal RBC

149
Q

what does the direct Coomb’s test test

A

if IgG is bound to the RBC

150
Q

pemphigus vulgaris is a type __ HSR

A

2

151
Q

what occurs with pemphigus vulgaris

A

IgG is produced against desmoglein proteins in desmosomes, leading to blisters and tissue destruction

152
Q

myasthenia gravis is an example of a type __ HSR

A

2

153
Q

what occurs with myasthenia gravis

A

antibody against a receptor at the neuromuscular junction causes loss of cell function

154
Q

goodpasture syndrome is an example of a type __ HSR

A

2

155
Q

what occurs with goodpasture syndrome

A

antibodies bind to glomerular basement membrane in kidneys/lungs causing destruction through phagocytosis granule release

156
Q

what is an Arthus reaction

A

the result of a localized inflammation of the small vessels (i.e., vasculitis) near the injection of antigen due to the interaction between the injected antigens and the circulating antibodies IgG which are created after repeated exposure to a specific antigen.
As a result, immune complexes are formed around and within the blood vessels of the skin. Subsequently, activation of the complement cascade, which is part of the innate immune system, enhances the local inflammation.
type 3 HSR

157
Q

how are immune complexes normally cleared

A

complexes are carried to the spleen/liver to be phagocytosed

158
Q

what causes serum sickness

A

injection of non-human serum into a human causes IgG made against the non-human serum
complement is activated and immune complex formation is formed, which is not cleared by the liver/spleen quick enough

159
Q

what are the 4 symptoms of serum sickness

A

fever
arthralgia (achy joints)
lymphadenopathy
skin eruption (rashes)

160
Q

is serum sickness a fast or slow response

A

slow due to production of IgG and complement activation

161
Q

what is extrinsic allergic alveolitis

A

repeated inhalation of an antigen causes IgG production
results in complement activation and inflammation

162
Q

what is the cause of lupus symptoms

A

autoantibody and immune complex deposition

163
Q

lupus is a type __ HSR

A

3

164
Q

in lupus, anti-dsDNA antibodies will be present where, causing the most evident symptoms

A

in cells with rapid turnover

165
Q

hyperacute graft rejection is __ immunity while acute is __ immunity

A

hyperacute= humoral (B cell antibody)
acute= cellular/adaptive (T cell) or humoral (if complement is deposited)

166
Q

what is involved in the prescreening before a graft transplant

A

prescreen recipient for existing antibody reaction to different HLA proteins to determine how reactive the patient is to different proteins

167
Q

what are some reasons for ischemia/reperfusion injury during graft transplant

A

death of donor brainstem induces hemodynamic and neuroendocrine responses
there may be a period of warm ischemia after cardiac death
cell swelling and toxic metabolite buildup during cold storage
further injury due to rapid warming following revascularization

168
Q

what is a consequence of tissue damage caused by ischemia/reperfusion injury

A

activation of autoreactive T and B cells, leading to further inflammation and graft damage

169
Q

what is clinical operational tolerance

A

a solid organ transplant recipient exhibits a well functioning graft and lacks histological signs of rejection after receiving no immunosuppression for at least 1 year

170
Q

what are 4 mechanisms associated with tolerance following a graft transplant

A

deletion of alloreactive T cells
anergy
immunoregulation
clonal exhaustion (T cells get exhausted and give up)

171
Q

bone marrow transplants involve CD __ cell transplant

A

CD34+ (stem cells)

172
Q

in graft vs. host disease, what are the 3 main organs affected

A

skin
liver
gut

173
Q

graft vs. host disease is believed to be mediated by what cells in the graft

A

mature donor T cells

174
Q

what are neoantigens

A

tumor antigens

175
Q

is an immune response made against cancer

A

yes, macrophages and lymphocytes (CD8+ T cells) infiltrate, however it doesn’t always work

176
Q

how do cytotoxic T cells (CD8+ T cells) become sensitized to tumor antigens

A

antigen presenting cells present tumor antigen

177
Q

what occurs to antigen presenting cells when there is tumor development

A

APC convert to being regulatory
*they calm T cell response instead of activating

178
Q

____ antibodies are being used to attack cancer cells

A

monoclonal antibodies

179
Q

what is involved with checkpoint blockade for immune evasion by tumor cells

A

Checkpoint proteins, such as PD-L1 on tumor cells and PD-1 on T cells, help keep immune responses in check. The binding of PD-L1 to PD-1 keeps T cells from killing tumor cells in the body. Blocking the binding of PD-L1 to PD-1 with an immune checkpoint inhibitor (anti-PD-L1 or anti-PD-1) allows the T cells to kill more, including to kill tumor cells. Suppression of the T cell response is relieved

Immune checkpoints are a normal part of the immune system. Their role is to prevent an immune response from being so strong that it destroys healthy cells in the body.

180
Q

what are chimeric antigen receptor T cells (CAR T cells) for use in cancer (usually blood cell cancers)

A

A patient’s T cells are changed in the laboratory so they will bind to cancer cells and kill them
The gene for a special receptor called a chimeric antigen receptor (CAR) is inserted into the T cells in the laboratory. Millions of the CAR T cells are grown in the laboratory and then given to the patient by infusion. The CAR T cells are able to bind to an antigen on the cancer cells and kill them.

181
Q

what is natural active immunity

A

direct exposure to the antigen (“in the wild”)

182
Q

what is artificial active immunity

A

intentional exposure through vaccine

183
Q

what is natural passive immunity

A

transfer of antibodies from mother to baby through placenta (IgG) or through breast milk (IgA)

184
Q

what is artificial passive immunity

A

injection of purified antibody, antibody containing serum (pooled plasma/serum), or sensitized cells

185
Q

what is involved in neutralization of virus with vaccines

A

antibody binds to protein on viral surface that would otherwise bind to proteins on host cells

186
Q

what are AB exotoxins

A

toxins released from an antigen
contains A site and B site
B chain attached to binding side on host cell, allowing for entry through phagocytosis

187
Q

what is involved with viral neutralization through AB exotoxin using a vaccine

A

antibody binds to the B subunit of an A/B endotoxin, preventing bind and phagocytosis of the exotoxin

188
Q

what are the 2 classes of whole organism vaccines

A

live attenuated
whole killed

189
Q

what are live attenuated vaccines

A

a selected for microbe has the same epitopes as the pathogenic strain, but is unable to cause disease
replication of virus in vaccine is possible

190
Q

what are whole killed vaccines

A

a microbe that causes disease is killed but still has the same epitopes
no replication is possible

191
Q

what are 3 subunit vaccine types in which the whole organism isn’t used

A

acellular
toxoid
anti-capsular

192
Q

what are acellular subunit vaccines

A

proteins known to be important for pathogenicity are used

193
Q

what are toxoid subunit vaccines

A

an inactivated version of an A/B exotoxin are used through modification of the B binding subunit

194
Q

what are anti-capsular subunit vaccines

A

the carbohydrate used in capsules is used along with a complexed protein

195
Q

what are live attenuated vaccines used for

A

protection requiring T cell immune response and/or a secreted IgA response

196
Q

what is the most effective vaccine form

A

live attenuated
*they look like the actual antigen and replicate at the actual site of the antigen

197
Q

what are whole killed vaccines used for

A

microbes that can’t be attenuated or microbes with oncogenic potential

198
Q

what are adjuvants

A

material added to subunit/toxoid vaccines to increase immunogenocity
(prolongation of antigen persistence, enhancement of so-stimulation signals, induction of localized inflammation)

199
Q

acellular boredtella pertussis vaccine and hepatitis B vaccine are examples of what type of vaccine

A

subunit

200
Q

DTaP is an example of what type of vaccine

A

toxoid

201
Q

what is sertotype replacement

A

vaccinating against one type of capsule doesn’t give the selected advantage against another type of capsule

202
Q

how do RNA viruses work

A

the vaccine contains pieces of mRNA packed into a lipid that can slide into cell
once inside the cell, mRNA attached with ribosome to make protein against the virus

203
Q

what is herd immunity

A

the idea that not everyone needs to be vaccinated to gain protection against a disease, as long as they’re surrounded by people who are immune to the disease

Immunology (4 decks)

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