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Immunology-Spring 2017 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What are pathogen antigens brought to the draining lymph node by?

A

Dendritic cells

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2
Q

How do blood born antigens enter the spleen?

A

Via the blood

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3
Q

What does inflammation increase?

A

Drainage of fluid into lymph

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4
Q

What do dendritic cells present antigen to? Where?

A

T cells

In T cell areas

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5
Q

What is a naive T cell?

A

T cells that have not yet encountered their antigen

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6
Q

What are effector T cells?

A

T cells that have been activated and can carry out their function

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7
Q

What are lymph nodes linked through?

A

Lymphatic vessels

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8
Q

What are the 2 routes the naive T cells can enter the draining lymph node?

A

In the blood

In the afferent lymph coming from an upstream lymph node

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9
Q

What do T cells sample?

A

Antigen presented on dendritic cells

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10
Q

During an infection, what happens to antigen specific T cells?

A

They are trapped in draining lymph node very efficiently

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11
Q

What can dendritic cells process antigen through? (3)

A 
MHC class I
MHC class II
Cross presentation pathways
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12
Q

What does receptor mediated endocytosis of bacteria activate?

A

MHC class II

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13
Q

What does macropinocytosis of bacteria of viruses activate?

A

MHC Class II

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14
Q

What does a viral infection activate?

A

MHC class I

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15
Q

What does cross-presentation of exogenous viral antigens activate?

A

MHC class I

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16
Q

What are 2 ways that dendritic cells become activated in the presence of an infection?

A

Pathogen PAMPs binding to dendritic cell PRRs

Inflammatory cytokines produced during an inflammatory response

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17
Q

After activation, what do dendritic cells do? (3)

A

Synthesize the co-stimmulatory molecule B7
Increase antigen processing and presentation on MHC molecules
Upregulate the chemokine receptor CCR7

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18
Q

What is activation of a T cell for the first time called?

A

Priming

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19
Q

What are the 3 signals that T cell activation requires?

A
  1. The T-cell receptor complex binds to peptide:MHC
  2. CD28 binds to costimulatory molecule B7
  3. Cytokines
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20
Q

What is needed for T cell proliferation?

A

IL-2

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21
Q

What is differentiation to one of the 5 CD4 T cell subsets determined by?

A

Cytokines

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22
Q

What do naive T cell express a low affinity for?

A

IL-2 receptor

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23
Q

What are activated T cells induced to express?

A

A high affinity IL-2 receptor and secrete IL-2

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24
Q

What are drugs that inhibit IL-2 production used as?

A

Immunosuppressive drugs

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25
Q

What happens to an antigen presenting cell presenting self peptide?

A

They would not be activated to displace the co-stimulatory B7 molecule and would not activate T cells

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26
Q

What do effector CD8 T cells do?

A

Kill cells infected with intracellular pathogen

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27
Q

What does an infected cell display?

A

Antigens on MHC class I molecules

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28
Q

What cells will cytotoxic T cells kill?

A

Any that display the same antigen that activated the T cell

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29
Q

After it has been activated, what does the T cell no longer require?

A

A co-stimulatory signal

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30
Q

What do T cells form with their target cell?

A

A conjugate pair

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31
Q

What are cytokines and cytotoxins delivered through?

A

A synapse

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32
Q

What do CD8 T cells secrete to activate macrophages?

A

IFN-γ

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33
Q

What do cytotoxins produce?

A

A pore in the target cell membrane

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34
Q

What are granzymes delivered through?

A

Pores

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35
Q

What do granzymes activate?

A

Capases

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36
Q

What does the granzyme target cell undergo?

A

Apoptosis

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37
Q

What does perforin do?

A

Aids in delivering contents of granules into the cytoplasm of target cell

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38
Q

What do granzymes do?

A

Activate apoptosis once in the cytoplasm of the target cell

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39
Q

What are the 5 different classes of helper T cells?

A 
Th1 cells
Th2 cells 
Th17 cells
Tfh cells
Treg cells
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40
Q

What is the function of Th1 cells?

A

Activate macrophages

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41
Q

What is the function of Th17 cells?

A

Enhance neutrophil response

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42
Q

What is the function of Th2 cells?

A

Activate cellular and antibody response to parasites

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43
Q

What are the functions of Tfh cells?

A

Activate B cells

Maturation of antibody response

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44
Q

What is the function of Treg cells?

A

Suppress other effector cells

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45
Q

What do Th1 cells further stimulate macrophages to do?

A

Destroy the material in their intracellular vesicles

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46
Q

What does a Th1 cells and a macrophage form?

A

A conjugate pair

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47
Q

What are the 2 signals required by macrophages for further activation?

A

IFN-γ

CD40L

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48
Q

What does CD40L do?

A

Binds CD40 on the macrophages

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49
Q

When do granulomas form?

A

When an intracellular pathogen can’t be totally eliminated

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50
Q

What does the granuloma do?

A

Walls off the pathogen and prevents dissemination throughout the body

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51
Q

What is linked recognition?

A

B cell and T cell receptors recognize different epitopes on the same antigen

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52
Q

What does the activation of B cells require?

A

Binding CD40 to CD40L

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53
Q

What are cytokines required for?

A

Class switching

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54
Q

What are the responses that Th2 cells promote mediated by?

A

Eosinophils
Mast cells
IgE

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55
Q

What do Th2 cells promote?

A

Bodily functions aimed to flush out the parasite

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56
Q

What does the promotion of bodily fluids by Th2 cells cause? (4)

A 
Increased:
Mucus production
Diarrhea
Vomiting
Smooth muscle contraction
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57
Q

What do Th17 cells protect agains?

A

Extracellular bacteria and fungi

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58
Q

When were Th17 cells discovered?

A

2007

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59
Q

What are Th17 cells found?

A

In the mucosal immune system

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60
Q

How much of the Treg cells are natural Treg cells?

A

15%

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61
Q

Where and when are natural Treg cells produced?

A

In the thymus during T cell development

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62
Q

What do some T cells that are negatively selected become?

A

Tregs

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63
Q

What do induced Tregs differentiate from?

A

Naive CD4 T cells in the periphery

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64
Q

What are naive CD4 T cells induced to become Tregs by?

A

Anti-inflammatory cytokines

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65
Q

What do γ:δ T cells maintain?

A

Tissue integrity

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66
Q

What do γ:δ T cells recognize?

A

Antigens that distinguish stressed cells from healthy cells

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67
Q

What do γ:δ T cells kill?

A

Infected/damaged cells

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68
Q

What do γ:δ T cells promote?

A

Tissue repair

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69
Q

What is the majority type of T cells in tissues? How much of these make up the T cell population in blood?

A

γ:δ T cells

5%

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70
Q

What do γ:δ T cells participate in?

A

Innate defense against microbes

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71
Q

What do γ:δ T cells produce?

A

Inflammatory cytokines and antimicrobial peptides

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72
Q

What do γ:δ T cells not recognize?

A

Peptide on MHC

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73
Q

What do γ:δ T cells respond quickly to?

A

Stress/infections similar to an innate response

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74
Q

Do γ:δ T cells show less or more receptor diversity than α:β cells?

A

Less

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75
Q

How many people does severe combined immunodeficiency (SCID) affect?

A

1 in 100,000

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76
Q

What is SCID also known as?

A

Bubble boy disease

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77
Q

What is SCID?

A

No functional T cells

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78
Q

What are 3 causes of SCID?

A

IL-2R mutation
RAG protein mutation
Abnormal thymic development

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79
Q

What is the role of T cells?

A

Function in all aspects of adaptive immunity

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80
Q

What are symptoms to SCID?

A

Extreme sensitivity to all types of infections

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81
Q

What is the treatment for SCID?

A

Hematopoietic stem cell transplantation gene therapy

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82
Q

What does HIV do?

A

Gradually depletes the body’s CD4 T cells

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83
Q

When does HIV become AIDS?

A

When CD4 T cell numbers become too low to provide adaptive immune responses

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84
Q

What does AIDS stand for?

A

Acquired immunodeficiency syndrome

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85
Q

Chapter 8 study guide and graphs

A

Chapter 8 study guide and graphs

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86
Q

What are the 3 signals for B cells?

A
  1. Binding of B cell receptor to its antigen
  2. Binding of B cell co-receptor to complement factor C3d
  3. Linked antigen recognition by cognate T cell
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87
Q

What does the dimerization of receptors induce?

A

A signal transduction pathway

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88
Q

In signal 2, what does CR1 induce?

A

Cleavage of C3b on pathogen surface to iC3b and C3d

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89
Q

In signal 2, what does CR2 bind?

A

C3d

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90
Q

In signal 2, what does CD19 associate with? What does it enhance?

A

B cell receptor complex

Signaling

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91
Q

What do the B cell receptor and co-receptor do together?

A

Act synergistically to initiate B cell activation

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92
Q

What does a T cell provide in signal 3?

A

CD40L and cytokines

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93
Q

What does CD40L do?

A 
Helps induce B cell proliferation
Promotes class switching and somatic hypermutation
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94
Q

What do different cytokines determine?

A

Antibody class

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95
Q

What does a B cell form a cognate pair with?

A

T cell that recognizes a linked peptide

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96
Q

What drives B cell proliferation?

A

CD40L and IL-4

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97
Q

What do the long processes that follicular dendritic cells have, have?

A

Complement receptors and Fc receptors

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98
Q

What do follicular dendritic cells capture?

A

Intact antibody/antigen/complement complexes for presentation to B cells

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99
Q

What do subcapsular sinus macrophages present?

A

Intact antigens on complement receptors

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100
Q

What do B cells that do not encounter a cognate T cell undergo?

A

Apoptosis

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101
Q

What do B cells that have bound antigen do?

A

Move to the boundary region to find a newly activated cognate Tfh cell

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102
Q

Where do conjugate pairs move to first? Why?

A

The medullary cords

To form a primary focus

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103
Q

What do some B cells differentiate to?

A

Plasma cells secreting low affinity IgM antibody

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104
Q

What do some other B cells do?

A

Leave and move back to the follicles to form a germinal center

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105
Q

What do germinal center B cells undergo?

A

Somatic hypermutation and class switching

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106
Q

What does movement to the germinal center result in?

A

High affinity class switched antibodies

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107
Q

After binding to the antigen, how long does the adaptive immune response take?

A

5 days

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108
Q

What does the dark zone of germinal centers have?

A

Centroblasts

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109
Q

What happens in the dark zone?

A

Rapidly proliferating B cells undergoing somatic hypermutation

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110
Q

In the dark zone, what is the expression of surface immunoglobulin receptors like?

A

Low

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111
Q

What does the light zone of germinal centers contain? (3)

A

Centrocytes
High density follicular dendritic cells
Tfh cells

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112
Q

What happens in the light zones?

A

B cells proliferate slower and mutated immunoglobulin receptors are displayed

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113
Q

What do the high density FDCs and Tfh cells in light zones promote?

A

Selection and survival of the higher affinity B cells

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114
Q

How does selection of B cells occur in light zones?

A

In increments

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115
Q

What do B cells with low affinity receptors undergo? Why?

A

Apoptosis

Cannot compete for limited antigen

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116
Q

What are B cells with high affinity receptors signaled to do?

A

Survive

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117
Q

What is class switching determined by?

A

Cytokines

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118
Q

What does class switching require interactions between?

A

CD40 (B cell) and CD40L (T cell)

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119
Q

What do individuals that lack CD40L have?

A

Hyper IgM syndrome

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120
Q

What happens with hyper IgM syndrome?

A

They only secrete low affinity IgM and they do not undergo somatic hypermutation or class switching

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121
Q

Do B cell responses to thymus-independent (TI) antigens require T cell help?

A

No

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122
Q

What are many common bacterial antigens classified as?

A

TI antigens

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123
Q

What are the 2 types of TI antigens?

A

TI-1 antigens

TI-2 antigens

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124
Q

What do TI-1 antigens cause?

A

Polyclonal activation at high concentration

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125
Q

What does polyclonal activation cause?

A

Proliferation and differentiation of most B cells independent of antigen specificity

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126
Q

What are examples of TI-1 antigens?

A

LPS and bacterial DNA which activate TLRs expressed by B cells

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127
Q

At low concentration, what do TI-1 antigens cause?

A

Antigen specific T cell responses

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5
Perfectly
128
Q

What do TI-2 antigens consist of?

A

Highly repetitive structures

129
Q

What do TI-2 antigens provide?

A

A prompt response to capsulated bacteria

130
Q

What can TI-2 antigens activate?

A

Only mature B cells

131
Q

What are immature B cells inactivated by?

A

Repetitive epitopes

132
Q

What are TI-2 antigen responses made primarily by?

A

B-1 cells and marginal zone B cells of the spleen

133
Q

Do infants generate effective TI-2 antigen responses against polysaccharide antigens?

A

No

134
Q

What is the H. influenzae vaccine physically linked to?

A

Tetanus toxoid protein

135
Q

What does the H. influenzae vaccine physically generate?

A

A thymus-dependent B2 response

136
Q

What is the first antibody to be produced during an immune response?

A

IgM

137
Q

What kind of affinity does IgM have for an antigen? Why?

A

Low

It is produced prior to somatic hypermutation

138
Q

What does IgM form? Why?

A

Pentamers

To increase overall binding strength

139
Q

What are antibody classes other than IgM produced through?

A

Class switching in the germinal center

140
Q

What does class switching do?

A

Changes antibody function, but does not affect binding to antigen

141
Q

What is the most abundant antibody in serum?

A

IgG

142
Q

What makes IgG a good all-around antibody?

A

4 different subclasses with distinct functions

143
Q

What are the 4 different subclasses of IgG?

A

IgG1
IgG2
IgG3
IgG4

144
Q

What are 4 examples of monomers?

A

IgD
IgE
IgG
IgA

145
Q

What is an example of a dimer?

A

IgA

146
Q

What is an example of a pentamer?

A

IgM

147
Q

Look at shape of monomers, dimers, and pentamers

A

Look at shape of monomers, dimers, and pentamers

148
Q

What does IgG, monomeric IgA, and IgM do?

A

Protect extravascular tissues

149
Q

What is the most abundant class in blood?

A

IgG

150
Q

Why do IgG and IgA diffuse into tissue more easily than IgM?

A

They are smaller

151
Q

What does dimeric IgA do?

A

Protects mucosal surfaces

152
Q

What is the most abundant antibody class in the body?

A

Dimeric IgA

153
Q

What is IgG transported across?

A

The placenta

154
Q

How are antibodies from the mother delivered?

A

Across the placenta and in breast milk

155
Q

How are babies provided with IgA?

A

Through breast milk

156
Q

Why is it important the newborn babies get IgA through breast milk?

A

They do not have any to protect the extensive mucosal surfaces

157
Q

When does maternal IgG decline?

A

After birth

158
Q

When do infants start to make their own IgM?

A

Before birth

159
Q

What do infants start to make their own IgA?

A

Around 3 months

160
Q

What antibody is transported across epithelium?

A

Dimer IgA

161
Q

What antibodies are diffused into extravascular sites?

A

IgG 1-4

Monomer IgA

162
Q

What antibodies are high affinity neutralizing antibodies?

A

IgG 1-4

IgA

163
Q

What do high affinity neutralizing antibodies prevent?

A

Attachment of microbes, toxins, and venoms to epithelial surfaces

164
Q

What antibodies activate the classical complement pathway?

A

IgM and IgG

165
Q

How do IgM and IgG activated the classical pathway?

A

They bind to the pathogen surface and interact with C1q

166
Q

Do IgM and IgG interact with C1q when not bound to the pathogen surface?

A

No

167
Q

What binds IgE antibody?

A

Mast cells
Eosinophils
Basophils

168
Q

What does IgE do with mast cells?

A

Binds to Fcε receptors and awaits antigen binding

169
Q

What happens when IgE on mast cells binds antigen?

A

The mast cell secretes inflammatory mediators

170
Q

What does IgE act on?

A

Smooth muscle to promote physical expulsion of parasite

171
Q

What does IgE increase?

A

Blood vessel permeability to flush parasite out

172
Q

What does the binding of an eosinophil to an IgE coated parasite do?

A

Triggers exocytosis of granules

173
Q

What promotes antibody dependent cell mediated cytotoxicity?

A

Binding of IgG to Fcγ receptors on NK cells

174
Q

What do natural killer cells have a receptor for?

A

IgG

175
Q

What do NK cells recognize?

A

Host cells coated with IgG

176
Q

What promotes phagocytosis?

A

Binding of IgG antibody to Fcγ receptors

177
Q

How many people do X-linked agammaglobulinemia affect?

A

1 in 200,000

178
Q

What is X-linked agammaglobulinemia?

A

Defective B cells receptor signaling during B cell development results in no functional B cells

179
Q

What are symptoms of X-linked agammaglobulinemia?

A

Susceptible to infections with extracellular bacteria and fungi
Recurrent infections that can lead to tissue and organ damage

180
Q

What is treatment for X-linked agammaglobulinemia like?

A

Regular infusions of antibody

Antibiotic to treat infections

181
Q

How can hyper IgM syndromes happen? (2)

A

CD40L deficiency

Activation-induced cytidine deaminase deficiency

182
Q

How many people does the CD40L deficiency affect?

A

X linked, 2 in 1,000,000

183
Q

What are symptoms of a CD40L and activation-induced cytidine deaminase deficiencies?

A

Susceptible to infections with extracellular bacteria and fungi
Defective clearance of intracellular pathogens

184
Q

What are treatments for a CD40L and activation-induced cytidine deaminase deficiencies?

A

Regular infusions of antibody

Antibiotics to treat infections

185
Q

What happens in an activation-induced cytidine deaminase deficiency?

A

Lack of affinity maturation and class switching

186
Q

How many people does a selective IgA deficiency affect?

A

1 in 500 caucasians

187
Q

What happens in a selective IgA deficiency?

A

Individuals do not produce IgA antibodies and IgM compensates at mucosal surfaces

188
Q

What are symptoms of selective IgA deficiency?

A

Many do not have symptoms, but it is estimated that 25-50% of patients are more prone to infections

189
Q

Chapter 9 study guide and graphs

A

Chapter 9 study guide and graphs

190
Q

What do mucosal surfaces do?

A

Protect the gastrointestinal tract, respiratory tract, urogenital tract, and glands

191
Q

What is the structure of mucosal surfaces like?

A

Thin and permeable

192
Q

Where do the majority of pathogens enter the body?

A

Through mucosal surfaces

193
Q

What are mucosal surfaces populated by?

A

Commensal microbes

194
Q

What are mucins?

A

Glycosylated polypeptides found in mucus

195
Q

What are mucins cross-linked to form?

A

Large, extended molecules

196
Q

What do mucins do? (4)

A

Lubricates mucosal surfaces
Physically impedes microorganisms
Retains antibody and anti-microbial molecules
Turns-over every couple of days

197
Q

What are mucins produced by?

A

Goblet cells in the mucosal epithelium

198
Q

What are the major segments of the gastrointestinal tract?

A

Mouth
Stomach
Small intestine
Large intestin

199
Q

What are the mucosal surfaces of the GI tract protected by?

A

Gut associate lymphoid tissue (GALT)

200
Q

What comprises the GALT and mesenteric lymph nodes?

A

Secondary lymphoid tissues

201
Q

What does the GALT of the small intestine comprise?

A

Peyer’s patches
Isolated lymphoid follicles
Appendix

202
Q

What do paneth cell in the epithelium do?

A

Secrete antimicrobial substances

203
Q

What do microfold cells (M cells) do?

A

Transport microbial antigens from gut lumen to dendritic cells and lymphocytes in the Peyer’s patch

204
Q

What are paneth cells that main source of?

A

Defensins in the intestine

205
Q

What is an immune response characterized by?

A

Inflammation in non-mucosal tissues

206
Q

What contact do non-mucosal tissues have with microbes?

A

Only occasional contact

207
Q

Is there a proactive immune response in the non-mucosal tissues?

A

No

208
Q

What happens in non-mucosal tissues when the barrier is breached?

A

Tissue microphages promote an inflammatory response to attract effector cells to clear the infection

209
Q

What is the mucosal immune response to innocuous antigens like?

A

Anti-inflammatory

210
Q

What contact do mucosal tissues have with microbes?

A

Continuous contact

211
Q

How does the mucosal immune system make adaptive immune response against gut microbes?

A

Proactively so that it is prepared for a breach in the barrier

212
Q

Are effector lymphocytes present in the absence of an infection?

A

Yes

213
Q

How are antibodies produced against gut microbes?

A

Proactively

214
Q

What are other effector cells doing?

A

They are armed and waiting for a breach in the epithelial barrier

215
Q

What are intestinal macrophages classified as?

A

Phagocytic

216
Q

What happens to monocytes when the arrive in the lamina propria from blood?

A

They lose their inflammatory potential

217
Q

Do intestinal macrophages perform inflammatory functions associated with systemic tissue macrophages?

A

No

218
Q

Do intestinal macrophages secrete inflammatory cytokines?

A

No

219
Q

What do intestinal macrophages not express?

A

T cell co-stimulatory molecules in order to become activated

220
Q

What is the default response to innocuous antigens?

A

Anti-inflammatory

221
Q

What do intestinal dendritic cells promote?

A

Tolerance to food antigens

222
Q

What do the intestinal dendritic cells move to and do?

A

Move to mesenteric lymph node and activate Tregs

223
Q

What do the dendritic cells secrete?

A

Retinoic acid

224
Q

What does retinoic acid play an important role in?

A

Promoting tolerance

225
Q

What is oral tolerance?

A

Tolerance of non-microbial protein antigens taken in through the oral route

226
Q

What happens in oral tolerance?

A

Systemic and mucosal immune systems become unresponsive

227
Q

What can dendritic cells do with the lumen?

A

Extend across the epithelial layer to capture antigens from the lumen of the gut

228
Q

What is the steady-state response to commensal microbes?

A

Non-inflamamtory

229
Q

In the absence of infection, wha does the mucosal immune system produce?

A

Proactive anti-inflammatory immune responses against antigens in the gut

230
Q

What must the mucosal immune system be able to distinguish and react appropriately to? (3)

A

Harmless, non-microbial antigens
Commensal microbial antigens
Pathogen microbial antigens

231
Q

What do intestinal dendritic cells in the secondary lymphoid tissue promote?

A

A non-inflammatory response to commensals

232
Q

Is the response from intestinal dendritic cells the same as oral tolerance to food antigens?

A

No

233
Q

What does the steady-state response to commensals involve? (3)

A

Activation of Tregs to keep other T cells in check
Activation of some other effector T cell subsets kept in check by the Tregs
Activation of B cells to produce IgA

234
Q

What does the uptake and presentation of non-invasive microbes by intestinal dendritic cells generate?

A

Plasma cells secreting IgA

235
Q

What does the detection of microbial PAMPs by epithelial cells do?

A

Stimulates constitutive production of antimicrobial proteins

236
Q

What is the primary function of IgA?

A

Neutralization

237
Q

Are inflammatory immune cells and molecules present in the lumen of the gut?

A

No

238
Q

What is antigen presentation like in the mucosal immunes system?

A

Can be anti-inflammatory or inflammatory depending on the environment

239
Q

What do anti-inflammatory cytokines in the microenvironment do?

A

Promote Treg differentiation and IgA production

Dampen inflammatory responses

240
Q

What does invasion by opportunistic commensal or pathogens result in?

A

An inflammatory response

241
Q

What can intestinal epithelial cells do?

A

Sense a breach and activate the immune response

242
Q

What can toll-like receptors do?

A

Sense bacteria that penetrate the mucosal layer and epithelium

243
Q

What do NOD receptors do?

A

Sense bacteria that breach the epithelial layer

244
Q

What do compromised epithelial cells secrete?

A

Inflammatory cytokine

245
Q

What does the pro-active nature of the mucosal immune system allow for?

A

Infections to be dealt with promptly

246
Q

What is associated with inappropriate inflammation of mucosal tissue?

A

Diseases

247
Q

What happens during celiac disease?

A

Pro-inflamatory responses are generated against gluten

248
Q

What happens during Crohn’s disease?

A

Pro-inflammatory responses against commensal bacteria

249
Q

What are 3 anatomical features of the mucosal immune system?

A

Intimate interactions between n=mucosal epithelia and lymphoid tissues
Discrete compartments of diffuse lymphoid and more organized structures
Specialized antigen-uptake mechanisms provided by M cells

250
Q

What are 2 effector mechanisms of the mucosal immune system?

A

Activated effector T cells predominate even in the absence of infection
Plasma cells are in the tissues where antibodies are needed

251
Q

What is the immunoregulatory environment of the mucosal immune system like? (2)

A

Dominant and active down regulation of inflammatory immune response to food and other innocuous environmental antigens
Inflammation-anergic macrophages and tolerance-inducing dendritic cells

252
Q

Chapter 10 study guide and graphs

A

Chapter 10 study guide and graphs

253
Q

What is the course a typical acute infection? (4)

A
  1. Establishment of infection
  2. Induction of adaptive response
  3. Adaptive immune response
  4. Immunological memory
254
Q

What is protective memory?

A

High antibody levels are sustained for several months after an infection is cleared

255
Q

What is the low steady-state level of antibody maintained indefinitely by?

A

Long-lived plasma cells

256
Q

What is the secondary adaptive immune response?

A

The immune response against second and subsequent exposure to antigen

257
Q

Where are clones of B cells and T cells produced?

A

In the primary immune response

258
Q

What is the process of cloning T cells? (3)

A
  1. Naive T cell is activated by pathogen
  2. A clone of pathogen-specific effector and memory T cells is produced
  3. Effect T cells outnumber memory T cells
259
Q

What is the process of cloning B cells? (3)

A
  1. Naive B cell is activated by the pathogen and a Tfh cel
  2. A clone of pathogen-specific B cell is produced
  3. Effector B cells outnumber memory B cells
260
Q

What do memory B cells and memory T cells provide?

A

Long-lived protection

261
Q

In individuals 1-75 after receiving a small pox vaccination that were analyzed, what was shown?

A

Many individuals retained memory T cells up to 50 and 75 years after vaccination

262
Q

What was the half life of memory T cells measured to be?

A

8-12 years

263
Q

After the small pox vaccination, what were the antigen specific antibody levels like?

A

The remained stable between 1-75 years after vaccination

264
Q

What is the half life of antigen specific antibodies?

A

Cannot be determined

265
Q

Were antibody levels correlated with the number memory T cells?

A

No

266
Q

What are characteristics of memory B cell response? (4)

A

Protective memory is provided by low-level antigen specific antibody produced by long-lived plasma cells Reactive memory is provided by memory B cells
More antigen specific memory B cells compared to the initial number of antigen specific naïve cells
Memory B cells have already undergone class switching and somatic hypermutation
Memory B cells are preferentially activated over new naïve B cells that would produce lower affinity antibody

267
Q

Why are memory B cells activated earlier?

A

It takes less antigen

268
Q

What do memory B cells immediately produce?

A

Class switched high affinity antibodies

269
Q

What do memory B cells undergo with subsequent exposure to antigen?

A

Further somatic hypermutation and affinity maturation

270
Q

With exposure to antigen, what happens to the affinity of antibody for the antigen?

A

It continues to rise

271
Q

What do B cells become more efficient at?

A

Presenting antigen to cognate T cells

272
Q

What does B cells presenting antigen to cognate T cells mean?

A

Less pathogen is need to initiate B cell response

Memory B cells take less time to differentiate to plasma cells

273
Q

What happens to memory Cells and naive B cells during the secondary response?

A

Memory B cells are activated and naive B cells are inhibited

274
Q

What do naive B cells have during the secondary response?

A

An inhibitory Fcγ receptor

275
Q

What does the binding of the antigen/antibody complex to the B cell receptor and inhibitory receptor do?

A

Delivers inhibitory signals to the naive B cells

276
Q

How many lack the RhD erythrocyte antigen?

A

16% of caucasian mothers

277
Q

What do RhD-ve mothers generate?

A

Anti-RhD antibodies against fetus erythrocytes that cross the placenta

278
Q

What can the primary immune response be inhibited by in mothers?

A

Administering anti-RhD antibody

279
Q

What antibodies do people tend to make?

A

Those only against the epitopes expressed on the initial pathogen encounter

280
Q

What happens to the strength of the memory response with each infection by a new strain?

A

It declines

281
Q

What are 2 memory T cell characteristics?

A

Effector memory T cells circulate in peripheral tissues and are already differentiated and ready to provide protective memory
Central memoryT cells circulate in secondary lymphoid tissues

282
Q

What are central memory T cells like compared to naive T cells? (2)

A

Undifferentiated, but more readily activated

Start producing cytokines earlier

283
Q

What is a vaccination?

A

A deliberate immunization that can elicit a primary immune response, but has little pathogenic potential

284
Q

What is the goal of vaccination?

A

To develop long lasting immunological memory

285
Q

What was the first medically prescribed vaccine against?

A

Smallpox

286
Q

What was the overall historical fatality rate of smallpox?

A

30%

287
Q

When was smallpox declared eradicated?

A

1979

288
Q

How does the smallpox vaccine work? (3)

A

Cowpox and smallpox share some surface antigens
Immunization with cowpox induces antibodies against cowpox surface antigens
Cowpox antibodies bund to and neutralize the smallpox virus

289
Q

What was the practice of immunization prior to the 19th century? What was used?

A

Variolation

Dried material from pustule of a mild infection

290
Q

In the 19th century, what was used as a vaccine for smallpox?

A

Cowpox virus

291
Q

Since the 20th century, what has been used to vaccinate against smallpox?

A

Vaccina virus

292
Q

What are the 3 types of vaccines?

A

Live attenuated vaccine
Inactivated vaccine
Subunit vaccine

293
Q

How are live-attenuated vaccines produced?

A

By growing in cells from another species

294
Q

What are the steps to producing a live attenuated vaccine with another species, such as monkey cells?

A

The pathogenic virus is isolated from a patient and grown in human cultured cells
The cultured virus is used to infect monkey cells
The virus acquires a variety of mutations that allow to grow well in monkey cells
The virus no longer grows well in human cell and can be used as a vaccine

295
Q

What does attenuated mean?

A

It becomes less and less able to grow in human cells causing reduced pathogenicity

296
Q

What can happen to live-attenuated pathogens in immunocompromised individuals?

A

They may retain the ability to revert back to a pathogenic form

297
Q

Can killed/inactivated viruses replicate?

A

No

298
Q

Why are inactivated viruses not as effected as live attenuated vaccines?

A

They don’t mimic a natural infection

299
Q

Has polio been eradicated?

A

In most countries, but it remains endemic in Afghanistan, Pakistan, and Nigeria

300
Q

What vaccine is preferred in countries where risk of polio remains high?

A

Live-vaccine

301
Q

What vaccine for polio is recommended for use in the US?

A

Inactivated vaccine

302
Q

How does an oral live-attenuated vaccine respond to polio?

A

It provides stronger immunity, but carries the risk of reversion

303
Q

What are subunit vaccine?

A

Do not contain whole cells, but contain only antigens that best stimulate the immune system

304
Q

What are examples of subunit vaccines? (4)

A

Hepatitis B
TDaP
HPC
Meningitis C

305
Q

What are 2 consideration for peptide subunit vaccines?

A

May have to contain an adjuvant

Must contain a range of antigenic peptides that can bind a large number of MHC molecules

306
Q

What is an adjuvant?

A

A substance that stimulate the innate immune system

307
Q

What are conjugated vaccines important for?

A

Infants who elicit weak T cell independent responses to capsular polysaccharides

308
Q

What is the reversion rate of the polio vaccine like in the US for the live-attenuated vaccine?

A

It is deemed unacceptable

309
Q

What did the B. Pertussis (whooping cough) cause?

A

Killed whole-cell Pertussis vaccine caused pain, swelling, and fever

310
Q

What is now used for whooping cough?

A

Acellular vaccines with fewer adverse effects

311
Q

How many people does the small pox vaccine cause serious side effects in?

A

About 1 in 1 million

312
Q

What led to a reduced rate of the measles vaccination?

A

Suggested link between measles and autism

313
Q

What led to a reduced rate of Pertussis vaccination?

A

Suggested link between the vaccine and brain damage

314
Q

What is herd immunity?

A

A large majority of immune individuals protect a small minority of non-immune individuals

315
Q

What does herd immunity allow for? (2)

A

A smaller probability that non-immuneindividuals will come into contact with the pathogen
Chains of infected are disrupted

316
Q

What do decreased vaccination rates cause?

A

A loss of herd immunity

317
Q

What are some considerations for vaccine development? (2)

A

Must be perceived to be safe with minimal side effects

Must protect a large proportion of the population

318
Q

What are practical considerations for vaccine development? (3)

A

Research development and testing are expensive for pharmaceutical companies
Vaccine must be profitable to the company, but cheap for the consumers
Route of delivery

319
Q

Chapter 11 study guide and graphs

A

Chapter 11 study guide and graphs

Immunology-Spring 2017 (4 decks)

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