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OLD "MIC 660" > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What are the 3 populations of B cells?

A
  1. B-1
  2. B-2
  3. Marginal Zone B cells
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2
Q

Where do B-1 B cells usually reside?

A

body cavities

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3
Q

What is the primary job of B-1 B cells?

A

protect gut and lung tissue

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4
Q

Where are B-1 B cells generated?

A

fetal liver (self-renewing)

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5
Q

Does B-1 B cells have diversity?

A

Not much; no VDJ recombination or class switching

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6
Q

Do B-1 B cells require T helper cells for activation?

A

No (T cell independent)

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7
Q

B-1 B cell primary produce the _____ isotype

A

IgM

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8
Q

Do B-1 B cells produce memory B cells?

A

No

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9
Q

Where do B-2 B cells reside?

A

most parts of the body

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10
Q

What population of B cells makes up most of the B cell population?

A

B-2

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11
Q

Where are B-2 B cells generated?

A

bone marrow

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12
Q

Do B-2 B cells require Helper T cells for activation?

A

yes (T dependent)

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13
Q

Do B-2 B cells produce memory B cells?

A

yes

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14
Q

Do B-2 B cells have diversity?

A

yes; undergo class switching and recombination

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15
Q

What isotypes can B-2 B cells produce?

A

All the Igs

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16
Q

Where do marginal-zone B cells reside?

A

marginal zone of spleen

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17
Q

What is the purpose of marginal-zone B cells?

A

bloodborne pathogens

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18
Q

What isotypes can marginal zone B cells produce?

A

mainly IgM
sometimes IgG

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19
Q

Where do B cells start and complete thier development?

A

start: Bone marrow
end: spleen

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20
Q

What is the commitment signal for B cells in the bone marrow?

A

IL-7

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21
Q

___________ expresses IL-7 while _________ expresses IL-7R

A

bone marrow
lymphoid precursor

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22
Q

What are the 8 Stages of B-2 cell development

A
  1. Early Pro-B
  2. Late Pro-B
  3. Large Pre-B
  4. Small Pre-B
  5. Immature B
  6. Transitional 1
  7. Transitional 2
  8. Mature B cell
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23
Q

What happens during Early Pro-B stage?

A

Heavy chain D+J rearrangement

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24
Q

What happens during Late Pro-B stage?

A

Heavy chain V+DJ rearrangement

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25
Q

What is used to check the heavy chain rearrngment?

A

surrogate light chain

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26
Q

What is the surrogate light chain made of?

A

VpreB
gamma5

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27
Q

When and what are the checkpoints for B-2 recombination?

A

1st: test for heavy chain function (after late pro B)
2nd: test for functional B cell receptor (after small pre B)

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28
Q

What does the VpreB part of the surrogate light chain mimic?

A

variable region of light chain

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29
Q

What does the gamma5 part of the surrogate light chain mimic?

A

constant region of light chain

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30
Q

After the surrogate light chain is used to check if the heavy chain is working, the heavy chain forms a complex with Ig alpha and Ig beta to test for ….

A

ability to form Pre-B cell receptor

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31
Q

What happens during Large Pre-B cell stage?

A

allelic exclusion of the heavy chain

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32
Q

What happens during the Small Pre-B cell stage?

A

light chain V+J recombination

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33
Q

What are the 2 possible light chain loci on B cells?

A

kappa
lambda

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34
Q

What happens during the immature B cell stage?

A

negative selection in bone marrow

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35
Q

Immature B cells in the bone marrow that recognize self-antigen have one of three fates….

A
  1. clonal deletion (apoptosis)
  2. receptor editing (another chance)
  3. anergy (nonresponsive)
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36
Q

Why is negative selection in B cells not as stringent compared to T cells?

A

B-2 don’t have AIRE so activation is dependent on helper T cells that themselves have already gone through very strict selection

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37
Q

When do B cells traffic out of the bone marrow to the spleen?

A

immature to transitional 1

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38
Q

What happens during the Transitional 1 B cell stage?

A

negative selection

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39
Q

During the second round of negative selection during T1; the B cells begin expressing low levels of ________

A

BAFF-R (survival factor)

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40
Q

What happens during transitional 2 B cell stage?

A

positive selection (post receptor editing)

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41
Q

During the T2 stage; B cells begin expressing higher levels of ________

A

BAFF-R (survival factor)

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42
Q

Where do mature B-2 cells go after development in the spleen?

A

circulatory system then enter secondary lymph tissue for activation

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43
Q

Do B-1 or B-2 B cells need BAFF signaling for survival?

A

B-2

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44
Q

Because the heavy chain of BCR are so short they require ______ and _______ to mediate signaling

A

Ig beta
Ig alpha

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45
Q

What is the first signal of naive B cell activation?

A

crosslinking of the BCR

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46
Q

What is cross linking in B cell activation?

A

binding of antigen induces BCRs to cluster on the B cell surface

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47
Q

BCR crosslinking induces the activation of _________ on the Ig alpha and Ig beta

A

ITAMS

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48
Q

What is the B cell coreceptor made of?

A

CR2
CD19
CD81

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49
Q

What does CR2 do in the B cell coreceptor?

A

binds with C3b on the pathogen causing signaling

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50
Q

What does CD19 do in the B cell coreceptor?

A

cytoplasmic domain that signals

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51
Q

What does CD81 do in the B cell coreceptor?

A

stabilizes the complex

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52
Q

What is the signal transduction steps of B cell activation?

A
  1. Lyn/Fyn/Blk
  2. ITAMs
  3. Syk
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53
Q

What does Syk induce in the signal transduction of B cells?

A

the three signaling pathways

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54
Q

What are the three signaling pathways for B cells?

A

NFAT
NFkB
AP-1

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55
Q

Some B-2 B cells generate a ____________ and differentiate into plasma cells that produce soluble IgM

A

primary focus

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56
Q

Some B-2 B cells generate a ______________ and will become a memory B cell or plasma cell encoding high affinity antibodies of isotypes other than IgM and IgD

A

germinal centers

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57
Q

T-independent 1 antigens do crosslinking with BCR and co-receptor and express ______

A

PRR

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58
Q

T-independent 2 antigens do excessive ____________ of BCR and co-receptors

A

crosslinking

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59
Q

What T-independent B antigen uses PRR (TLR) as well as BCR to drive B cell activation?

A

TI-1 antigen

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60
Q

Which T independent antigen doesn’t require a secondary signal?

A

TI-2 (uses excessive crosslinking of BCR and co-receptor)

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61
Q

What 2 signals does T-dependent B cells require for activation?

A
  1. BCR and co-receptor signaling
  2. CD40 signaling (CD40L expressed on helper T cell)
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62
Q

How does T-dependent B cell activation work?

A

T helper cells position themselves on the boarder of the B cell follicles and interact with B cells to activate them

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63
Q

What is it called when T-dependent B cell’s peptide/MHC II complex is recognized by a helper T cell?

A

conjugate pair

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64
Q

When T-dependent B cell’s peptide/MHC II complex is recognized by a helper T cell, CD40-CD40L signaling induces the expression of __________ on B cells and ______ on T cells tightening the binding of the conjugate pair?

A

ICAM-1
LFA-1

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65
Q

What does the creation of a conjugate pair induce?

A

cytokine signaling for activation

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66
Q

What are the 2 fates of the conjugate pair?

A
  1. pair can migrate to medulla to become a primary focus
  2. pair can migrate back to primary lymph follicle to form a germinal center
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67
Q

What do B cells in a primary focus do?

A

differentiate into plasmablast that expresses IgM

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68
Q

What do B cells in germinal centers do?

A

AID is up regulated = somatic hypermutation in the CDR

(change the affinity of the BCR)

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69
Q

Centroblast migrate to the light zone to become ___________ where positive selection occurs

A

centrocytes

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70
Q

Do you want centrocytes to express high or low affinity of BCR?

A

high

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71
Q

Does negative and positive selection occur in the germinal center?

A

yes

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72
Q

Where does class switching occur for TD B cells?

A

germinal centers

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73
Q

________ on TFH binds with _______ on centrocytes during the selection process which induces AID and class switching in germinal centers

A

CD40L
CD40

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74
Q

What do centrocytes differentiate into?

A

plasma cells or memory B cells

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75
Q

What does the Fc fragment of antibodies do?

A

attaches to other immune cells

76
Q

What does the Fab fragment of antibodies do?

A

antigen binding region

77
Q

What are the loci of the light chain of an antibody?

A

lambda
kappa

78
Q

What are the heavy chain isotypes of antibodies?

A

all the Igs

79
Q

Do surface bound of secreted BCR initiate signaling pathways?

A

surface bound

80
Q

The heavy chain of each isotype of antibodies differ how?

A
  1. varying number of constant regions
  2. level of glycosylation
  3. length of hinge region
81
Q

What does the level of glycosyaltion of an antibodies Fc constant region determine?

A

which Fc receptors it can bind

82
Q

Where is the hinge region on an antibody?

A

where the Y arms come together

83
Q

What does the hinge region of an antibody allow?

A

Fab flexability

84
Q

What is the first 2 isotypes expressed by mature naive B cells?

A

IgM
IgD

85
Q

Soluble IgM form pentamers connected by a ___________

A

J chain

86
Q

What is the purpose of IgM?

A
  1. neutralize
  2. activate classical pathway
87
Q

What is the purpose of IgD?

A
  1. induce mast cells and basophils (degranulation)
88
Q

What is the purpose of IgA?

A
  1. protect mucosal surfaces
  2. neutralize
89
Q

Ig___ can come as a dimer or momer

A

IgA

90
Q

What Ig protects breast milk?

A

IgA

91
Q

What is the most abundant isotype?

A

IgG

92
Q

What Ig protects the fetus?

A

IgG

93
Q

Why are there some any different types of IgG?

A

differing hinge regions of diversity

94
Q

What is the purpose of IgG?

A
  1. neutralize
  2. opsonization
  3. classical complement

EVERYTHING

95
Q

How is IgG “bispecific”?

A

is can mix one heavy chain and light chain dimer with another heavy and light chain dimer

96
Q

What is the purpose of IgE?

A
  1. combat inhaled and ingested pathogens
  2. activate granulocytes
97
Q

What Ig isotype is involved with allergies?

A

IgE

98
Q

What isotypes neutralize?

A

G
A
M

99
Q

What isotypes opsonize (phagocytosis)?

A

G (especially IgG1 and 2)
A

100
Q

What isotypes activate complement?

A

G
A
M

101
Q

What isotypes activate innate immune cells (granulocytes) ?

A

D
E
G

102
Q

What isotypes protect internal tissues?

A

G
A
M

103
Q

What isotype activates NK cells?

A

IgG

104
Q

How do IgG antibodies kill pathogens?

A

recruit NK cells and induce antibody-dependent cell-mediated cytotoxicity

105
Q

IgA, M, and G protect interal tissues using _________

A

transcytosis

106
Q

IgA, M, and G protect against __________ pathogens

A

bloodborne

107
Q

Epithelial cells lining mucosal surfaces express __________ that covalently binds to dimeric IgA via its J chain; engulfing the antibody

A

poly-Ig

108
Q

The classical pathway can be activated by _______ instead of CRP

A

antibodies (IgM and G)

109
Q

IgM or IgG binding to a soluble multivalent antigen allowing C1 binding forms a ___________ complex

A

immune complex

110
Q

Immune complex bind with _____ and are recognized by RBC and travel through the liver and spleen where macrophages clear the complex (part of the activation of complement)

A

C3b

111
Q

What are the 2 severe combined immunodeficiencies (SCID)?

A
  1. Omenn syndrome
  2. ADA deficiency
112
Q

What are the 3 B cell specific immunodeficiencies?

A
  1. X-linked agammaglobulinemia
  2. Hyper-IgM syndrome
  3. selective IgA deficiency
113
Q

What is Omenn syndrome?

A

mutation in Rag1/2 = no recombination

114
Q

What is ADA deficiency?

A

deficient in ADA = inhibits cell proliferation = increased dATP

115
Q

What is X-linked agammaglobulinemia?

A

mutation in Btk = no survival signal sent

116
Q

What is Hyper-IgM syndrome and why is the defect in?

A

defect in CD40
defect in IKK
defect in AID
= blocks class switching

117
Q

What is Selective IgA deficiency?

A

lack of IgA making mucosal surfaces vulnerable

118
Q

What are 2 acquired B cell immunodeficiencies?

A
  1. B cel leukemia (pushes out healthy cells)
  2. Alcohol (lowers number of B cell)
119
Q

What are the 3 type II hypersensitivities?

A
  1. Goodpasture Syndrome
  2. Hashimoto Syndrome
  3. Myasthenia gravis
120
Q

What are the 2 type III hypersensitivities?

A
  1. Systemic Lupus Erythematosus (SLEE)
  2. Rheumatoid arthritis (RA)
121
Q

What is Goodpasture Syndrome?

A

destruction of basement membranes of kidney and lungs

122
Q

What is Hashimoto Disease?

A

destruction of thyroid epithelial cells via antibody-dependent cell-mediated cytotoxicity

123
Q

What is Myasthenia gravis?

A

acetylcholine receptor is blocked

124
Q

What is Systemic Lupus Erythematosus (SLE)?

A

targeted destruction communication cells causing tissue damage

125
Q

What is Rheumatoid Arthritis (RA)?

A

formation immune complexes in joints

126
Q

What is Multiple Sclerosis (MS)?

A

EBV infection and mimics GlyCAM affecting the CNS

cant tell the difference between self and virus

127
Q

What is Type II hypersensitivity?

A

autoantibodies of IgM or IgG binding cell surface molecules

128
Q

What is Type III hypersensitivity?

A

prouction of small immune complexes made of IgM or IgG that cannot be cleared

129
Q

How does the adaptive immune response differ when exposed a second time?

A

the response is stronger and fast

130
Q

The goal of vaccination is to form a _________ immunity (lessens disease) not a ___________ immunity (prevent infection)

A

protective
sterilizing

131
Q

Upon primary exposure to a pathogen, it can take up to _____ days to clear an infection

A

14 days

132
Q

Why is the primary response slow?

A

needs to coordinate the different arms of the immune system

133
Q

Are naive or memory cells long lived?

A

memory

134
Q

Are naive or memory cells easier to activate?

A

memory

135
Q

What are the 4 memory T cells?

A
  1. T SCM (stem memory)
  2. T CM (central memory)
  3. T EM (effector memory)
  4. T RM (resident memory(
136
Q

What is the first memory T cell produced during clonal expansion?

A

T SCM (T memory stem cells)

137
Q

Where do T SCM exist?

A

circulatory and lymph tissue

138
Q

What memory T cell is pluripotent?

A

T SCM

139
Q

What 2 types of memory T cells comes from T SCM?

A

T CM
T EM

140
Q

What T memory cell is self renewing?

A

T SCM

141
Q

Where do T CM exist?

A

circulatory and lymph tissue

142
Q

What is the job of T CM memory cells?

A

scan for antigen presenting DC in secondary lymph tissue

143
Q

T CM memory cells express high levels of ______ allow for activation of effector T cells

A

IL-2

144
Q

Where can T EM memory T cells exist?

A

anywhere in body

145
Q

T EM memory T cells can quickly activate and differentiate into effector T cells because they secrete ____ and _____

A

INF-g
TNF-a

146
Q

______ memory T cells can migrate close to site of infection preventing tissue from future infection

A

T EM

147
Q

Where do T RM memory cells reside?

A

tissue of origin

148
Q

What can T EM memory cells differentiate into?

A

T RM

149
Q

T RM have the same function as ______ memory T cells

A

T EM

150
Q

What are the 2 main sources of memory B cells?

A
  1. germinal center dependent
  2. germinal center independent
151
Q

Do germinal center dependent or independent memory B cells undergo somatic hypermutation and class switching?

A

germinal center dependent

152
Q

Are germinal center dependent or independent memory B cells more specialized and diverse?

A

germinal center dependent (undergo class switching)

153
Q

During the secondary immune response the activation of _________ is limited

A

naive B cells (too general need more specialized response; high affinity class switching antibodies)

154
Q

How is naive B cells inhibited during secondary immune response?

A

IgG bound to pathogen interacts with Fc-gamma-RIIB1 on naive B cells

155
Q

Why are vaccine challenging to design?

A

most pathogens do not have a closely related nonpathogenic counterparts (like small pocks)

156
Q

What are inactivated vaccines?

A

pathogen that is killed or inactivated

157
Q

What are live attenuated vaccines?

A

weakened pathogen

158
Q

What is an advantage of live attenuated vaccines?

A

most pathogen antigens are capable or producing a primary immune response

159
Q

What is a disadvantage of live attenuated vaccines?

A

cannot be given to immunocompromised people

160
Q

What are toxoid vaccines?

A

generate a primary immune response to toxins produced by pathogens

161
Q

What are subunit vaccines?

A

neutralizing antibodies bind to intracellular pathogens’ adhesion molecules blocking virus from binding to host cells

162
Q

What are conjugate vaccinees?

A

weak antigen with a stronger antigen (requires a non-protein antigen to stimulate IgG) like polysaccharides

163
Q

What is a advantage to conjugate vaccines?

A

young children and the elderly (they have a reduced amount of T-cell independent response to polysaccharides)

164
Q

What are adjuvants?

A

retain antigen and slowly release it allowing for a maintained innate response that isn’t cleared as quickly which can build a better immune response

165
Q

What are recombinant vector vaccines (viral vector vaccines)?

A

attenuated (weakened) virus infects host and uses it transcription/translation machinery to express pathogenic proteins

166
Q

What are DNA vaccines?

A

virus is used as a carrier for pathogen genes carried in an expression plasmid

167
Q

What is messenger RNA vaccines?

A

mRNA molecules that encodes a pathogenic protein packed in lipid nanoparticles and delivered to the cytoplasm of cell where mRNA is translated into protein and induces immune response

168
Q

monovalent antigens result in __________ while multivalent results in ___________ or __________

A

anergy

clonal deletion or receptor editing

169
Q

Where does peripheral and center tolerance happen for B-2 B cells?

A

central:bone marrow
peripheral: spleen

170
Q

TI-1 antigens require BCR signaling and _________

A

PRR

171
Q

What is the B cell receptor complex made of?

A

heavy chain
light chain
Ig alpha
Ig beta

172
Q

What must T-dependent B cells present on MHC II to helper T cells?

A

proteins

173
Q

What is the fate of plasmablasts?

A

primary focus (no class switching)

174
Q

BLIMP-1 is required for ….

A

B cells to become plasma cells

175
Q

centroblasts migrate to light zone and turn into __________ where they are tested for high affinity

A

centrocytes

176
Q

Once centrocytes are tested for high affinity, what happens to them?

A

cytokines are released to promote class switching

177
Q

Ig___ can form a pentamer connected by a J chain

A

IgM

178
Q

Why are IgM pentamers useful?

A

increases affinity since there are more binding sites

179
Q

What Ig is the most diverse?

A

IgG

180
Q

Ig___ and Ig___ activate the classical pathway once they go through a conformational change

A

IgM and IgG

181
Q

Where will most B cells be removed with Omenn Syndrome?

A

first checkpoint

182
Q

Where will most B cells be removed with X-linked agammaglobulinemia?

A

2nd checkpoint

183
Q

high affinity antibodies inhibit _______ B cells

A

naive

184
Q

Is the polio (salk) or polio (saban) more dangerous and why?

A

Saban (live attenuated) is more effective but its more dangerous

185
Q

What is an example of an adjuvant?

A

ISCOMS
lipid carriers encapsulate viral protein and deliver to cytoplasm allowing presentation on MHC I (which is difficult to do)

OLD "MIC 660" (10 decks)

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