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
What happens to an antigen presenting cell presenting self peptide?
They would not be activated to displace the co-stimulatory B7 molecule and would not activate T cells
26
What do effector CD8 T cells do?
Kill cells infected with intracellular pathogen
27
What does an infected cell display?
Antigens on MHC class I molecules
28
What cells will cytotoxic T cells kill?
Any that display the same antigen that activated the T cell
29
After it has been activated, what does the T cell no longer require?
A co-stimulatory signal
30
What do T cells form with their target cell?
A conjugate pair
31
What are cytokines and cytotoxins delivered through?
A synapse
32
What do CD8 T cells secrete to activate macrophages?
IFN-γ
33
What do cytotoxins produce?
A pore in the target cell membrane
34
What are granzymes delivered through?
Pores
35
What do granzymes activate?
Capases
36
What does the granzyme target cell undergo?
Apoptosis
37
What does perforin do?
Aids in delivering contents of granules into the cytoplasm of target cell
38
What do granzymes do?
Activate apoptosis once in the cytoplasm of the target cell
39
What are the 5 different classes of helper T cells?
``` Th1 cells Th2 cells Th17 cells Tfh cells Treg cells ```
40
What is the function of Th1 cells?
Activate macrophages
41
What is the function of Th17 cells?
Enhance neutrophil response
42
What is the function of Th2 cells?
Activate cellular and antibody response to parasites
43
What are the functions of Tfh cells?
Activate B cells | Maturation of antibody response
44
What is the function of Treg cells?
Suppress other effector cells
45
What do Th1 cells further stimulate macrophages to do?
Destroy the material in their intracellular vesicles
46
What does a Th1 cells and a macrophage form?
A conjugate pair
47
What are the 2 signals required by macrophages for further activation?
IFN-γ | CD40L
48
What does CD40L do?
Binds CD40 on the macrophages
49
When do granulomas form?
When an intracellular pathogen can't be totally eliminated
50
What does the granuloma do?
Walls off the pathogen and prevents dissemination throughout the body
51
What is linked recognition?
B cell and T cell receptors recognize different epitopes on the same antigen
52
What does the activation of B cells require?
Binding CD40 to CD40L
53
What are cytokines required for?
Class switching
54
What are the responses that Th2 cells promote mediated by?
Eosinophils Mast cells IgE
55
What do Th2 cells promote?
Bodily functions aimed to flush out the parasite
56
What does the promotion of bodily fluids by Th2 cells cause? (4)
``` Increased: Mucus production Diarrhea Vomiting Smooth muscle contraction ```
57
What do Th17 cells protect agains?
Extracellular bacteria and fungi
58
When were Th17 cells discovered?
2007
59
What are Th17 cells found?
In the mucosal immune system
60
How much of the Treg cells are natural Treg cells?
15%
61
Where and when are natural Treg cells produced?
In the thymus during T cell development
62
What do some T cells that are negatively selected become?
Tregs
63
What do induced Tregs differentiate from?
Naive CD4 T cells in the periphery
64
What are naive CD4 T cells induced to become Tregs by?
Anti-inflammatory cytokines
65
What do γ:δ T cells maintain?
Tissue integrity
66
What do γ:δ T cells recognize?
Antigens that distinguish stressed cells from healthy cells
67
What do γ:δ T cells kill?
Infected/damaged cells
68
What do γ:δ T cells promote?
Tissue repair
69
What is the majority type of T cells in tissues? How much of these make up the T cell population in blood?
γ:δ T cells | 5%
70
What do γ:δ T cells participate in?
Innate defense against microbes
71
What do γ:δ T cells produce?
Inflammatory cytokines and antimicrobial peptides
72
What do γ:δ T cells not recognize?
Peptide on MHC
73
What do γ:δ T cells respond quickly to?
Stress/infections similar to an innate response
74
Do γ:δ T cells show less or more receptor diversity than α:β cells?
Less
75
How many people does severe combined immunodeficiency (SCID) affect?
1 in 100,000
76
What is SCID also known as?
Bubble boy disease
77
What is SCID?
No functional T cells
78
What are 3 causes of SCID?
IL-2R mutation RAG protein mutation Abnormal thymic development
79
What is the role of T cells?
Function in all aspects of adaptive immunity
80
What are symptoms to SCID?
Extreme sensitivity to all types of infections
81
What is the treatment for SCID?
Hematopoietic stem cell transplantation gene therapy
82
What does HIV do?
Gradually depletes the body's CD4 T cells
83
When does HIV become AIDS?
When CD4 T cell numbers become too low to provide adaptive immune responses
84
What does AIDS stand for?
Acquired immunodeficiency syndrome
85
Chapter 8 study guide and graphs
Chapter 8 study guide and graphs
86
What are the 3 signals for B cells?
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
87
What does the dimerization of receptors induce?
A signal transduction pathway
88
In signal 2, what does CR1 induce?
Cleavage of C3b on pathogen surface to iC3b and C3d
89
In signal 2, what does CR2 bind?
C3d
90
In signal 2, what does CD19 associate with? What does it enhance?
B cell receptor complex | Signaling
91
What do the B cell receptor and co-receptor do together?
Act synergistically to initiate B cell activation
92
What does a T cell provide in signal 3?
CD40L and cytokines
93
What does CD40L do?
``` Helps induce B cell proliferation Promotes class switching and somatic hypermutation ```
94
What do different cytokines determine?
Antibody class
95
What does a B cell form a cognate pair with?
T cell that recognizes a linked peptide
96
What drives B cell proliferation?
CD40L and IL-4
97
What do the long processes that follicular dendritic cells have, have?
Complement receptors and Fc receptors
98
What do follicular dendritic cells capture?
Intact antibody/antigen/complement complexes for presentation to B cells
99
What do subcapsular sinus macrophages present?
Intact antigens on complement receptors
100
What do B cells that do not encounter a cognate T cell undergo?
Apoptosis
101
What do B cells that have bound antigen do?
Move to the boundary region to find a newly activated cognate Tfh cell
102
Where do conjugate pairs move to first? Why?
The medullary cords | To form a primary focus
103
What do some B cells differentiate to?
Plasma cells secreting low affinity IgM antibody
104
What do some other B cells do?
Leave and move back to the follicles to form a germinal center
105
What do germinal center B cells undergo?
Somatic hypermutation and class switching
106
What does movement to the germinal center result in?
High affinity class switched antibodies
107
After binding to the antigen, how long does the adaptive immune response take?
5 days
108
What does the dark zone of germinal centers have?
Centroblasts
109
What happens in the dark zone?
Rapidly proliferating B cells undergoing somatic hypermutation
110
In the dark zone, what is the expression of surface immunoglobulin receptors like?
Low
111
What does the light zone of germinal centers contain? (3)
Centrocytes High density follicular dendritic cells Tfh cells
112
What happens in the light zones?
B cells proliferate slower and mutated immunoglobulin receptors are displayed
113
What do the high density FDCs and Tfh cells in light zones promote?
Selection and survival of the higher affinity B cells
114
How does selection of B cells occur in light zones?
In increments
115
What do B cells with low affinity receptors undergo? Why?
Apoptosis | Cannot compete for limited antigen
116
What are B cells with high affinity receptors signaled to do?
Survive
117
What is class switching determined by?
Cytokines
118
What does class switching require interactions between?
CD40 (B cell) and CD40L (T cell)
119
What do individuals that lack CD40L have?
Hyper IgM syndrome
120
What happens with hyper IgM syndrome?
They only secrete low affinity IgM and they do not undergo somatic hypermutation or class switching
121
Do B cell responses to thymus-independent (TI) antigens require T cell help?
No
122
What are many common bacterial antigens classified as?
TI antigens
123
What are the 2 types of TI antigens?
TI-1 antigens | TI-2 antigens
124
What do TI-1 antigens cause?
Polyclonal activation at high concentration
125
What does polyclonal activation cause?
Proliferation and differentiation of most B cells independent of antigen specificity
126
What are examples of TI-1 antigens?
LPS and bacterial DNA which activate TLRs expressed by B cells
127
At low concentration, what do TI-1 antigens cause?
Antigen specific T cell responses
128
What do TI-2 antigens consist of?
Highly repetitive structures
129
What do TI-2 antigens provide?
A prompt response to capsulated bacteria
130
What can TI-2 antigens activate?
Only mature B cells
131
What are immature B cells inactivated by?
Repetitive epitopes
132
What are TI-2 antigen responses made primarily by?
B-1 cells and marginal zone B cells of the spleen
133
Do infants generate effective TI-2 antigen responses against polysaccharide antigens?
No
134
What is the H. influenzae vaccine physically linked to?
Tetanus toxoid protein
135
What does the H. influenzae vaccine physically generate?
A thymus-dependent B2 response
136
What is the first antibody to be produced during an immune response?
IgM
137
What kind of affinity does IgM have for an antigen? Why?
Low | It is produced prior to somatic hypermutation
138
What does IgM form? Why?
Pentamers | To increase overall binding strength
139
What are antibody classes other than IgM produced through?
Class switching in the germinal center
140
What does class switching do?
Changes antibody function, but does not affect binding to antigen
141
What is the most abundant antibody in serum?
IgG
142
What makes IgG a good all-around antibody?
4 different subclasses with distinct functions
143
What are the 4 different subclasses of IgG?
IgG1 IgG2 IgG3 IgG4
144
What are 4 examples of monomers?
IgD IgE IgG IgA
145
What is an example of a dimer?
IgA
146
What is an example of a pentamer?
IgM
147
Look at shape of monomers, dimers, and pentamers
Look at shape of monomers, dimers, and pentamers
148
What does IgG, monomeric IgA, and IgM do?
Protect extravascular tissues
149
What is the most abundant class in blood?
IgG
150
Why do IgG and IgA diffuse into tissue more easily than IgM?
They are smaller
151
What does dimeric IgA do?
Protects mucosal surfaces
152
What is the most abundant antibody class in the body?
Dimeric IgA
153
What is IgG transported across?
The placenta
154
How are antibodies from the mother delivered?
Across the placenta and in breast milk
155
How are babies provided with IgA?
Through breast milk
156
Why is it important the newborn babies get IgA through breast milk?
They do not have any to protect the extensive mucosal surfaces
157
When does maternal IgG decline?
After birth
158
When do infants start to make their own IgM?
Before birth
159
What do infants start to make their own IgA?
Around 3 months
160
What antibody is transported across epithelium?
Dimer IgA
161
What antibodies are diffused into extravascular sites?
IgG 1-4 | Monomer IgA
162
What antibodies are high affinity neutralizing antibodies?
IgG 1-4 | IgA
163
What do high affinity neutralizing antibodies prevent?
Attachment of microbes, toxins, and venoms to epithelial surfaces
164
What antibodies activate the classical complement pathway?
IgM and IgG
165
How do IgM and IgG activated the classical pathway?
They bind to the pathogen surface and interact with C1q
166
Do IgM and IgG interact with C1q when not bound to the pathogen surface?
No
167
What binds IgE antibody?
Mast cells Eosinophils Basophils
168
What does IgE do with mast cells?
Binds to Fcε receptors and awaits antigen binding
169
What happens when IgE on mast cells binds antigen?
The mast cell secretes inflammatory mediators
170
What does IgE act on?
Smooth muscle to promote physical expulsion of parasite
171
What does IgE increase?
Blood vessel permeability to flush parasite out
172
What does the binding of an eosinophil to an IgE coated parasite do?
Triggers exocytosis of granules
173
What promotes antibody dependent cell mediated cytotoxicity?
Binding of IgG to Fcγ receptors on NK cells
174
What do natural killer cells have a receptor for?
IgG
175
What do NK cells recognize?
Host cells coated with IgG
176
What promotes phagocytosis?
Binding of IgG antibody to Fcγ receptors
177
How many people do X-linked agammaglobulinemia affect?
1 in 200,000
178
What is X-linked agammaglobulinemia?
Defective B cells receptor signaling during B cell development results in no functional B cells
179
What are symptoms of X-linked agammaglobulinemia?
Susceptible to infections with extracellular bacteria and fungi Recurrent infections that can lead to tissue and organ damage
180
What is treatment for X-linked agammaglobulinemia like?
Regular infusions of antibody | Antibiotic to treat infections
181
How can hyper IgM syndromes happen? (2)
CD40L deficiency | Activation-induced cytidine deaminase deficiency
182
How many people does the CD40L deficiency affect?
X linked, 2 in 1,000,000
183
What are symptoms of a CD40L and activation-induced cytidine deaminase deficiencies?
Susceptible to infections with extracellular bacteria and fungi Defective clearance of intracellular pathogens
184
What are treatments for a CD40L and activation-induced cytidine deaminase deficiencies?
Regular infusions of antibody | Antibiotics to treat infections
185
What happens in an activation-induced cytidine deaminase deficiency?
Lack of affinity maturation and class switching
186
How many people does a selective IgA deficiency affect?
1 in 500 caucasians
187
What happens in a selective IgA deficiency?
Individuals do not produce IgA antibodies and IgM compensates at mucosal surfaces
188
What are symptoms of selective IgA deficiency?
Many do not have symptoms, but it is estimated that 25-50% of patients are more prone to infections
189
Chapter 9 study guide and graphs
Chapter 9 study guide and graphs
190
What do mucosal surfaces do?
Protect the gastrointestinal tract, respiratory tract, urogenital tract, and glands
191
What is the structure of mucosal surfaces like?
Thin and permeable
192
Where do the majority of pathogens enter the body?
Through mucosal surfaces
193
What are mucosal surfaces populated by?
Commensal microbes
194
What are mucins?
Glycosylated polypeptides found in mucus
195
What are mucins cross-linked to form?
Large, extended molecules
196
What do mucins do? (4)
Lubricates mucosal surfaces Physically impedes microorganisms Retains antibody and anti-microbial molecules Turns-over every couple of days
197
What are mucins produced by?
Goblet cells in the mucosal epithelium
198
What are the major segments of the gastrointestinal tract?
Mouth Stomach Small intestine Large intestin
199
What are the mucosal surfaces of the GI tract protected by?
Gut associate lymphoid tissue (GALT)
200
What comprises the GALT and mesenteric lymph nodes?
Secondary lymphoid tissues
201
What does the GALT of the small intestine comprise?
Peyer's patches Isolated lymphoid follicles Appendix
202
What do paneth cell in the epithelium do?
Secrete antimicrobial substances
203
What do microfold cells (M cells) do?
Transport microbial antigens from gut lumen to dendritic cells and lymphocytes in the Peyer's patch
204
What are paneth cells that main source of?
Defensins in the intestine
205
What is an immune response characterized by?
Inflammation in non-mucosal tissues
206
What contact do non-mucosal tissues have with microbes?
Only occasional contact
207
Is there a proactive immune response in the non-mucosal tissues?
No
208
What happens in non-mucosal tissues when the barrier is breached?
Tissue microphages promote an inflammatory response to attract effector cells to clear the infection
209
What is the mucosal immune response to innocuous antigens like?
Anti-inflammatory
210
What contact do mucosal tissues have with microbes?
Continuous contact
211
How does the mucosal immune system make adaptive immune response against gut microbes?
Proactively so that it is prepared for a breach in the barrier
212
Are effector lymphocytes present in the absence of an infection?
Yes
213
How are antibodies produced against gut microbes?
Proactively
214
What are other effector cells doing?
They are armed and waiting for a breach in the epithelial barrier
215
What are intestinal macrophages classified as?
Phagocytic
216
What happens to monocytes when the arrive in the lamina propria from blood?
They lose their inflammatory potential
217
Do intestinal macrophages perform inflammatory functions associated with systemic tissue macrophages?
No
218
Do intestinal macrophages secrete inflammatory cytokines?
No
219
What do intestinal macrophages not express?
T cell co-stimulatory molecules in order to become activated
220
What is the default response to innocuous antigens?
Anti-inflammatory
221
What do intestinal dendritic cells promote?
Tolerance to food antigens
222
What do the intestinal dendritic cells move to and do?
Move to mesenteric lymph node and activate Tregs
223
What do the dendritic cells secrete?
Retinoic acid
224
What does retinoic acid play an important role in?
Promoting tolerance
225
What is oral tolerance?
Tolerance of non-microbial protein antigens taken in through the oral route
226
What happens in oral tolerance?
Systemic and mucosal immune systems become unresponsive
227
What can dendritic cells do with the lumen?
Extend across the epithelial layer to capture antigens from the lumen of the gut
228
What is the steady-state response to commensal microbes?
Non-inflamamtory
229
In the absence of infection, wha does the mucosal immune system produce?
Proactive anti-inflammatory immune responses against antigens in the gut
230
What must the mucosal immune system be able to distinguish and react appropriately to? (3)
Harmless, non-microbial antigens Commensal microbial antigens Pathogen microbial antigens
231
What do intestinal dendritic cells in the secondary lymphoid tissue promote?
A non-inflammatory response to commensals
232
Is the response from intestinal dendritic cells the same as oral tolerance to food antigens?
No
233
What does the steady-state response to commensals involve? (3)
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
What does the uptake and presentation of non-invasive microbes by intestinal dendritic cells generate?
Plasma cells secreting IgA
235
What does the detection of microbial PAMPs by epithelial cells do?
Stimulates constitutive production of antimicrobial proteins
236
What is the primary function of IgA?
Neutralization
237
Are inflammatory immune cells and molecules present in the lumen of the gut?
No
238
What is antigen presentation like in the mucosal immunes system?
Can be anti-inflammatory or inflammatory depending on the environment
239
What do anti-inflammatory cytokines in the microenvironment do?
Promote Treg differentiation and IgA production | Dampen inflammatory responses
240
What does invasion by opportunistic commensal or pathogens result in?
An inflammatory response
241
What can intestinal epithelial cells do?
Sense a breach and activate the immune response
242
What can toll-like receptors do?
Sense bacteria that penetrate the mucosal layer and epithelium
243
What do NOD receptors do?
Sense bacteria that breach the epithelial layer
244
What do compromised epithelial cells secrete?
Inflammatory cytokine
245
What does the pro-active nature of the mucosal immune system allow for?
Infections to be dealt with promptly
246
What is associated with inappropriate inflammation of mucosal tissue?
Diseases
247
What happens during celiac disease?
Pro-inflamatory responses are generated against gluten
248
What happens during Crohn's disease?
Pro-inflammatory responses against commensal bacteria
249
What are 3 anatomical features of the mucosal immune system?
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
What are 2 effector mechanisms of the mucosal immune system?
Activated effector T cells predominate even in the absence of infection Plasma cells are in the tissues where antibodies are needed
251
What is the immunoregulatory environment of the mucosal immune system like? (2)
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
Chapter 10 study guide and graphs
Chapter 10 study guide and graphs
253
What is the course a typical acute infection? (4)
1. Establishment of infection 2. Induction of adaptive response 3. Adaptive immune response 4. Immunological memory
254
What is protective memory?
High antibody levels are sustained for several months after an infection is cleared
255
What is the low steady-state level of antibody maintained indefinitely by?
Long-lived plasma cells
256
What is the secondary adaptive immune response?
The immune response against second and subsequent exposure to antigen
257
Where are clones of B cells and T cells produced?
In the primary immune response
258
What is the process of cloning T cells? (3)
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
What is the process of cloning B cells? (3)
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
What do memory B cells and memory T cells provide?
Long-lived protection
261
In individuals 1-75 after receiving a small pox vaccination that were analyzed, what was shown?
Many individuals retained memory T cells up to 50 and 75 years after vaccination
262
What was the half life of memory T cells measured to be?
8-12 years
263
After the small pox vaccination, what were the antigen specific antibody levels like?
The remained stable between 1-75 years after vaccination
264
What is the half life of antigen specific antibodies?
Cannot be determined
265
Were antibody levels correlated with the number memory T cells?
No
266
What are characteristics of memory B cell response? (4)
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
Why are memory B cells activated earlier?
It takes less antigen
268
What do memory B cells immediately produce?
Class switched high affinity antibodies
269
What do memory B cells undergo with subsequent exposure to antigen?
Further somatic hypermutation and affinity maturation
270
With exposure to antigen, what happens to the affinity of antibody for the antigen?
It continues to rise
271
What do B cells become more efficient at?
Presenting antigen to cognate T cells
272
What does B cells presenting antigen to cognate T cells mean?
Less pathogen is need to initiate B cell response | Memory B cells take less time to differentiate to plasma cells
273
What happens to memory Cells and naive B cells during the secondary response?
Memory B cells are activated and naive B cells are inhibited
274
What do naive B cells have during the secondary response?
An inhibitory Fcγ receptor
275
What does the binding of the antigen/antibody complex to the B cell receptor and inhibitory receptor do?
Delivers inhibitory signals to the naive B cells
276
How many lack the RhD erythrocyte antigen?
16% of caucasian mothers
277
What do RhD-ve mothers generate?
Anti-RhD antibodies against fetus erythrocytes that cross the placenta
278
What can the primary immune response be inhibited by in mothers?
Administering anti-RhD antibody
279
What antibodies do people tend to make?
Those only against the epitopes expressed on the initial pathogen encounter
280
What happens to the strength of the memory response with each infection by a new strain?
It declines
281
What are 2 memory T cell characteristics?
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
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What are central memory T cells like compared to naive T cells? (2)
Undifferentiated, but more readily activated | Start producing cytokines earlier
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What is a vaccination?
A deliberate immunization that can elicit a primary immune response, but has little pathogenic potential
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What is the goal of vaccination?
To develop long lasting immunological memory
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What was the first medically prescribed vaccine against?
Smallpox
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What was the overall historical fatality rate of smallpox?
30%
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When was smallpox declared eradicated?
1979
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How does the smallpox vaccine work? (3)
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
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What was the practice of immunization prior to the 19th century? What was used?
Variolation | Dried material from pustule of a mild infection
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In the 19th century, what was used as a vaccine for smallpox?
Cowpox virus
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Since the 20th century, what has been used to vaccinate against smallpox?
Vaccina virus
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What are the 3 types of vaccines?
Live attenuated vaccine Inactivated vaccine Subunit vaccine
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How are live-attenuated vaccines produced?
By growing in cells from another species
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What are the steps to producing a live attenuated vaccine with another species, such as monkey cells?
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
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What does attenuated mean?
It becomes less and less able to grow in human cells causing reduced pathogenicity
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What can happen to live-attenuated pathogens in immunocompromised individuals?
They may retain the ability to revert back to a pathogenic form
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Can killed/inactivated viruses replicate?
No
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Why are inactivated viruses not as effected as live attenuated vaccines?
They don't mimic a natural infection
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Has polio been eradicated?
In most countries, but it remains endemic in Afghanistan, Pakistan, and Nigeria
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What vaccine is preferred in countries where risk of polio remains high?
Live-vaccine
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What vaccine for polio is recommended for use in the US?
Inactivated vaccine
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How does an oral live-attenuated vaccine respond to polio?
It provides stronger immunity, but carries the risk of reversion
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What are subunit vaccine?
Do not contain whole cells, but contain only antigens that best stimulate the immune system
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What are examples of subunit vaccines? (4)
Hepatitis B TDaP HPC Meningitis C
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What are 2 consideration for peptide subunit vaccines?
May have to contain an adjuvant | Must contain a range of antigenic peptides that can bind a large number of MHC molecules
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What is an adjuvant?
A substance that stimulate the innate immune system
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What are conjugated vaccines important for?
Infants who elicit weak T cell independent responses to capsular polysaccharides
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What is the reversion rate of the polio vaccine like in the US for the live-attenuated vaccine?
It is deemed unacceptable
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What did the B. Pertussis (whooping cough) cause?
Killed whole-cell Pertussis vaccine caused pain, swelling, and fever
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What is now used for whooping cough?
Acellular vaccines with fewer adverse effects
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How many people does the small pox vaccine cause serious side effects in?
About 1 in 1 million
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What led to a reduced rate of the measles vaccination?
Suggested link between measles and autism
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What led to a reduced rate of Pertussis vaccination?
Suggested link between the vaccine and brain damage
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What is herd immunity?
A large majority of immune individuals protect a small minority of non-immune individuals
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What does herd immunity allow for? (2)
A smaller probability that non-immuneindividuals will come into contact with the pathogen Chains of infected are disrupted
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What do decreased vaccination rates cause?
A loss of herd immunity
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What are some considerations for vaccine development? (2)
Must be perceived to be safe with minimal side effects | Must protect a large proportion of the population
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What are practical considerations for vaccine development? (3)
Research development and testing are expensive for pharmaceutical companies Vaccine must be profitable to the company, but cheap for the consumers Route of delivery
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Chapter 11 study guide and graphs
Chapter 11 study guide and graphs