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Immunology > Lectures 12 + 13: B cells > Flashcards

Lectures 12 + 13: B cells Flashcards

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
Q

What does the delta constant region express

A

IgD

26
Q

What does alternative splicing allow B-2 B cells to have

A

Synthesize both IgM and IgD and can now be released from bone marrow

27
Q

Is B cell maturation antigen dependent or independent

A

Independent

28
Q

What do B-2 cells make

A

Effector and memory B cells

29
Q

What do B1 cells make

A

Effector Cells

30
Q

T-dependent B cell activation

A

Protein antigens that lead to B cell activation with helper T cells

31
Q

T-independent B cell activation

A

Non-protein antigens that lead to B cell activation without helper T cells

32
Q

Where do B2 cells reside and what do they respond to

A

Reside in follicle and respond to TD antigens

33
Q

Where are B1 cells located and what do they respond to

A

Located in mucosal tissue and pleural/peritoneal cavities and respond to TI antigens

34
Q

What attracts follicular B cells

A

Attracted to follicles by chemokines secreted by follicular dendritic cells

35
Q

If B cells are inactivated what happens

A

Exit the follicle following the S1P gradient

36
Q

What happens when a B cell recognizes a protein antigen

A

Becomes activated resulting in proliferation and differentiation into memory and effector B cells

37
Q

What are some things follicular B cells can undergo once activated

A

Class switching, affinity maturation and development of memory cells

38
Q

What is the first signal in B cell activation

A

1a. Aggregation of BCR’s to crosslink when antigen binds
1b. Antigen crosslink BCR with CR19/21 instead of needing two BCR’s

39
Q

What happens after B cells are activated by first signal

A

Migrate to outer edge of follicle into T cell zone and interact with Th cells and present antigen to T cell

40
Q

What is the second signal for B cell activation

A

Interaction with B cell and T cell with CD40L and CD40 and Th cytokine release (IL-4 causes proliferation)

41
Q

After activation and proliferation of B cells what happens

A

Rapidly differentiate into antibody producing plasma cells and migrate to extract follicular area, short lived plasma cells producing low affinity IgM

42
Q

After B cells migrate to extrafollicular space what happens

A

Undifferentiated B cells migrate back to follicle with extrafollicular T cells (TfH)- site of germinal reaction

43
Q

What is the germinal center reaction

A

Follicle B cells interact with FDC’s and TfH cells to undergo isotope switching and affinity maturation (somatic hypermutation)

44
Q

What directs class switching

A

TfH interaction via CD40-CD40L and cytokines

45
Q

What cytokine induces isotope switching to IgG

A

IFN-y

46
Q

What cytokine induces class switching to IgE

A

TNF-alpha

47
Q

What cytokine induces class switching to IgA

A

TNF-Beta

48
Q

What are the steps in class switching

A

Requires recombining of V region with different constant region

49
Q

What enzyme is responsible for class switching

A

Activation-induced cytidine deaminase (AIDs)

50
Q

How does the enzyme AIDs work

A

Intentionally introduces mutations

51
Q

What are the results of a deficiency in enzyme AIDS

A

Produces a normal or high concentrations of IgM with low IgA, IgG, IgE and patients have recurrent bacterial, respiratory and GI infections

52
Q

How does affinity maturation occur

A

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
Q

What occurs after affinity maturation

A

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
Q

High affinity follicular B cells differentiate into

A

Effector B (plasma) or memory cells

55
Q

What is the role of plasma cells

A

Make antibodies, no longer express MHC II or co-stimulatory molecules so can’t present antigen

56
Q

What does the activation of memory B cells result in

A

Secondary immune response

57
Q

What cells are activated in primary immune response

A

Naive B cells

58
Q

what Ig is synthesized in primary immune response

A

IgM then go through affinity maturation, class switching to IgE, IgG, IgA and produce memory cells

59
Q

What Ig is synthesized during secondary immune response

A

IgG no IgM
Affinity maturation occurs, creating higher affinity antibodies and more memory cells produced

60
Q

B1 cells serve as _____ against pathogens at mucosal tissues, pleural and peritoneal cavities

A

First line of defense

61
Q

How are B1 cells activated

A

Multivalent binding and cross-linking of BCR’s

Immunology (22 decks)

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