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Immunology > Lectures 12 + 13: B cells > Flashcards

Lectures 12 + 13: B cells Flashcards

(61 cards)

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1
Q

Effector B cells are ___

A

Antibody secreting plasma cells

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2
Q

What are the two subclasses of B cells

A

B1- primarily mature in fetal liver and can self renew
B2- follicular- mature in bone marrow

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3
Q

What does the transmembrane region of BCR interact with for signaling

A

CD79 (Ig-alpha and Ig-beta)

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4
Q

What is the BCR complex

A

BCR, Ig-alpha, Ig-beta
Expressed by all B cells and is important during signal transduction during antigen induced B cell activation

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5
Q

Where does B cell development occur

A

Bone marrow

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6
Q

What directs the development of B cells

A

Stromal cells in bone marrow

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7
Q

How are the gene segments of BCR made

A

Random somatic recombination

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8
Q

What is the early pro B cell stage

A

Rearrangement of D-J on heavy chain mediated by RAG 1 and RAG2

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9
Q

What is late pro B cell

A

Rearrangement of V-DJ on heavy chain

First start with V-DJ rearrangement on first chromosome- if successful signaled to survive
If not make V-DJ rearrangement on 2nd chromosome- if successful then survive if not apoptosis

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10
Q

What is the first checkpoint in B cell development

A

Large Pre-B cell to check functional HC with VpreB lambda5

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11
Q

What is Large Pre-B cell step

A

Checks for functional heavy chain and compatibility with surrogate light chain-VpreB lambda 5

If comparable will express and proliferate line

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12
Q

What is allelic exclusion and why is it important

A

Ensures B cells express only one receptor type, if expressed more would hinder response especially T-independent B cell activation that requires crosslinking

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13
Q

What is X-linked agammaglobulinemia

A

Mutation in BTK-serine kinase important for signal transduction in pre-B cell

Disease is characterized by lack of B cells and low serum antibodies

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14
Q

What is small Pre-B cell stage

A

V-J rearrangement on LC
Start with kappa and then move to lambda

V-J rearrangement on kappa gene on first chromosome, if successful=survive and make kappa,mu IgM if not try V-J rearrangement on kappa gene on 2nd chromosome if works=survive and kappa, mu on IgM

If rearrangement on kappa doesn’t work move to lambda gene, V-J rearrangement on lambda gene on first chromsome if works=survive and lambda mu IgM, if not try V-J rearrangement on 2nd chromosome if works=lambda mu IgM, if doesn’t=apoptosis

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15
Q

What is combinatorial diversity

A

What V, D, J rearrangements are used and how do heavy and light chains interct

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16
Q

What is junctional diversity

A

During splicing what nucleotides are added or removed

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17
Q

What happens after completing small pre B cell process

A

Result is immature B cell that enters negative selection

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18
Q

What is negative selection

A

Assess self-recognition and reactivity to self, if reacts to self either will undergo clonal deletion, receptor editing on V-J on LC, anergy or immunological ignorance

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19
Q

What is clonal deletion

A

Removal of cells of a specific antigen specificity

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20
Q

What is receptor editing

A

Further genetic rearrangement to replace BCR with one that doesn’t self react

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21
Q

What is anergy

A

Permanent state of unresponsiveness, eventuality leading to death

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22
Q

What is immunological ignorance

A

Cells have affinity for self antigens but do not response

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23
Q

What occurs after negative selection of B cells

A

Alternative RNA splicing to make a VDJ region with either a mu or delta constant region

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24
Q

What does the mu constant region express

A

IgM

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25
What does the delta constant region express
IgD
26
What does alternative splicing allow B-2 B cells to have
Synthesize both IgM and IgD and can now be released from bone marrow
27
Is B cell maturation antigen dependent or independent
Independent
28
What do B-2 cells make
Effector and memory B cells
29
What do B1 cells make
Effector Cells
30
T-dependent B cell activation
Protein antigens that lead to B cell activation with helper T cells
31
T-independent B cell activation
Non-protein antigens that lead to B cell activation without helper T cells
32
Where do B2 cells reside and what do they respond to
Reside in follicle and respond to TD antigens
33
Where are B1 cells located and what do they respond to
Located in mucosal tissue and pleural/peritoneal cavities and respond to TI antigens
34
What attracts follicular B cells
Attracted to follicles by chemokines secreted by follicular dendritic cells
35
If B cells are inactivated what happens
Exit the follicle following the S1P gradient
36
What happens when a B cell recognizes a protein antigen
Becomes activated resulting in proliferation and differentiation into memory and effector B cells
37
What are some things follicular B cells can undergo once activated
Class switching, affinity maturation and development of memory cells
38
What is the first signal in B cell activation
1a. Aggregation of BCR’s to crosslink when antigen binds 1b. Antigen crosslink BCR with CR19/21 instead of needing two BCR’s
39
What happens after B cells are activated by first signal
Migrate to outer edge of follicle into T cell zone and interact with Th cells and present antigen to T cell
40
What is the second signal for B cell activation
Interaction with B cell and T cell with CD40L and CD40 and Th cytokine release (IL-4 causes proliferation)
41
After activation and proliferation of B cells what happens
Rapidly differentiate into antibody producing plasma cells and migrate to extract follicular area, short lived plasma cells producing low affinity IgM
42
After B cells migrate to extrafollicular space what happens
Undifferentiated B cells migrate back to follicle with extrafollicular T cells (TfH)- site of germinal reaction
43
What is the germinal center reaction
Follicle B cells interact with FDC’s and TfH cells to undergo isotope switching and affinity maturation (somatic hypermutation)
44
What directs class switching
TfH interaction via CD40-CD40L and cytokines
45
What cytokine induces isotope switching to IgG
IFN-y
46
What cytokine induces class switching to IgE
TNF-alpha
47
What cytokine induces class switching to IgA
TNF-Beta
48
What are the steps in class switching
Requires recombining of V region with different constant region
49
What enzyme is responsible for class switching
Activation-induced cytidine deaminase (AIDs)
50
How does the enzyme AIDs work
Intentionally introduces mutations
51
What are the results of a deficiency in enzyme AIDS
Produces a normal or high concentrations of IgM with low IgA, IgG, IgE and patients have recurrent bacterial, respiratory and GI infections
52
How does affinity maturation occur
AID induced somatic hypermutation within gene segments encoding the variable domains of heavy and light chains Exposure to antigen leads to new round of affinity maturation (ex: why we do booster vaccines to re-up memory cells and induce somatic hyper mutation)
53
What occurs after affinity maturation
Mutation in proliferating B cells in follicle so they now express a BCR with either higher or lower binding affinity for original antigen and must be tested, those that have the highest binding affinity to antigen survive, those that don’t undergo apoptosis
54
High affinity follicular B cells differentiate into
Effector B (plasma) or memory cells
55
What is the role of plasma cells
Make antibodies, no longer express MHC II or co-stimulatory molecules so can’t present antigen
56
What does the activation of memory B cells result in
Secondary immune response
57
What cells are activated in primary immune response
Naive B cells
58
what Ig is synthesized in primary immune response
IgM then go through affinity maturation, class switching to IgE, IgG, IgA and produce memory cells
59
What Ig is synthesized during secondary immune response
IgG no IgM Affinity maturation occurs, creating higher affinity antibodies and more memory cells produced
60
B1 cells serve as _____ against pathogens at mucosal tissues, pleural and peritoneal cavities
First line of defense
61
How are B1 cells activated
Multivalent binding and cross-linking of BCR’s

Immunology (22 decks)

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