Chapter 12 - B Cells Part 2 Flashcards

0
Q

How many constant regions do IgE and IgM have?

IgA, IgD, IgG?

A

4

3

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1
Q

How do you transition from a membrane IgM to a secreted IgM?

A

lose transmembrane and cytoplasmic segments

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2
Q

What happens in the Fab region?

Fc portion?

A

Ag binding

Effector function

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3
Q

What is Ig class switching driven by and where does it happen?

what happens in Ig class switching?

A

by TFH cells in the GC

changing the Constant region of the heavy chain

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4
Q

TRUE or FALASE?

Antigen specificity is changed with class switching.

A

FALSE

variable region unchanged, but can interact with different effector molecules

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5
Q

B cells in mucosal tissues switch to what?

What cytokines stimulate the switch?

A

IgA

TGF-beta, BAFF

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6
Q

CD40 signals work to induce isotype switching with what enzyme?

what is the enzyme need for?

A

activation-induced deaminase (AID)

isotype switching and affinity maturation

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7
Q

immunodeficiencies are dominated by what Igs?

A

IgM

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8
Q

Where does CSR take place and what does it change?

A

activated B cells

changes CH gene

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9
Q

where does CSR take place between?

A

2 switch regions (S) with looped-out deletion

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10
Q

What is the CSR preceded by?

what do these structures open?

A

germline transcripts

the chromatin structure of a specific S region, recombinase can activate

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11
Q

explain the CSR mechanism

A

AID activated by CD40 and TFH cells
AID deaminates cytosine in ssDNA (C–>U)
UNG removes U, APE1 endonuclease creates nicks that lead to ds break

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12
Q

what is affinity maturation?

is it T-dependent or T-independent?

A

process that leads to increased affinity of Abs for a particular Ag

T-dependent protein

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13
Q

What is required for somatic mutation to be initiated?

A

CD40-CD40L and helper T cells

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14
Q

Where does somatic hypermutation occur and is of what type of genes?

what is the result?

A

GC, of Ig V genes

production of Abs with high affinity for Ag

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15
Q

In proliferating GC B cells in the dark zone, what is happening at an extremely high rate?

A

Ig V genes undergo point mutations

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16
Q

what is mutation in Ig V genes called?

A

somatic hypermutation

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17
Q

Where do mutations cluster?

what has more mutations: IgG or IgM?

A

in V regions, mostly in the Ag-binding CDRs

IgG

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18
Q

Where does B cell apoptosis occur?

What stimulates class switching?

A

GC

TFH

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19
Q

Where do B cells that have undergone somatic mutation migrate to?

A

the FDC-rich light zone of the GC

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20
Q

When are B cells with high-affinity receptors for the Ag best able to bind the Ag?

A

when the Ag is present at low [ ]’s by follicular DCs

21
Q

what are the B cell survival mechanisms?

A

1) Bcl-2 expression
2) Presentation of Ag for TFH cells in the GC which signal CD40L
3) High affinity B cells activate endogenous inhibitor of Fas

22
Q

Where do B cell lymphomas develop from?

what are they caused by?

A

GC B cells

chromosomal translocations of oncogenes into Ig gene loci

23
Q

what are the 2 types of plasma cells?

A

short lived and long lived

24
Q

What are the characteristics of short-lived plasma cells?

A

T-independent, extrafollicular, found in 2ndary lymphoid organs and peripheral non-lymphoid tissues

25
Q

what are the characteristics of long-lived plasma cells?

A

T-dependent

generated by signals from BCR and IL-21 via plasmablasts

26
Q

Where are plasmablasts generated? Where do they home?

A

GC, enter circulation to home to bone marrow and differentiate into long-lived plasma cells

27
Q

how are plasma cells maintained?

A

BAFF

28
Q

What % of Ab in the blood is produced by long-lived plasma cells?

A

50

29
Q

Where are memory cells generated from?

what do they express high levels of?

A

GC for T-dependent Ag

Bcl-2

30
Q

Memory cells typically express what kind of Ag receptors and what kind of Ig molecules?

A

high affinity (mutated) receptors

switched isotype molecules

31
Q

What do effective vaccines against microbes and toxins require?

A

affinity maturation AND memory B cell formation

32
Q

What are conjugate vaccines?

what do they more readily induce?

A

polysaccharides covalently linked to a foreign protein to form a hapten-carrier equivalent

high-affinity Abs and memory cells

33
Q

What are TI characteristics?

A

multivalent, low level isotype switching (IgM), little or no affinity maturation

34
Q

What are TD characteristics?

A

proteins, lots of isotype switching, allows affinity maturation and secondary responses

35
Q

How do TI Ags become activated with T cell help?

A

maximal cross-linking of the BCR complex on B cells

36
Q

Where are TI Ab responses initiated?

A

spleen, bone marrow, peritoneal cavity, and mucosal sites

37
Q

What kind of B cells are especially important for Ab responses to TI ags?

A

Marginal zone and B-1

38
Q

what do marginal zone b cells mainly respond to?

what do they differentiate into after activation?

A

polysaccharides

short-lived plasma cells that secrete IgM

39
Q

Where may TI Ags persist for long periods of time?

A

surface of marginal zone macrophages in the spleen

40
Q

What do B-1 cells respond to?

A

TI Ags in the peritoneum and mucosal sites

41
Q

What do TI Ags of polysaccharide nature activate?

A

complement system via alternate pathway

generate C3d, binds to Ag, recognized by CR2 on B cell

42
Q

what is the dominant Ab class induced by pneumococcal capsular polysaccharide?

A

IgG2

43
Q

BAFF produced by DCs and macrophages induces synthesis of what?

what facilitates this?

A

AID in Ag-activated B cells

activation of TLR on B cells

44
Q

what mediates IgA switching?

A

TGF-beta

45
Q

what is the major mechanism of host defense against infections by encapsulated bacteria?

A

humoral immunity

46
Q

what contributes to the generation of natural Ab?

A

TI Ags

47
Q

most Abs are ______ produced by ______ stimulated by _____

A

low affinity anti-carb Abs
peritoneal B-1 cells
Marginal Zone B cells in the spleen

48
Q

Blood group Ags are important for what but not important for what?

A

imp: blood transfusions and transplantation

NOT: host defense

49
Q

what do polysaccharide vaccines induce?

A

long-lived protective immunity

50
Q

what happens in b cell activation involving PIP3?

A

BCR –> PIP3 –> B cell activated

51
Q

what is the mechanism of the FcgammaRIIB receptor?

A

SHIP converts PIP3 –> PIP2 in BCR complex
this blocks b cell receptor signaling and there is no activation

phosphatases of the Fcg… tail inhibit signaling in the BCR complex