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 (Cā€“>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 [ ]ā€™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
What are the characteristics of short-lived plasma cells?
T-independent, extrafollicular, found in 2ndary lymphoid organs and peripheral non-lymphoid tissues
25
what are the characteristics of long-lived plasma cells?
T-dependent | generated by signals from BCR and IL-21 via plasmablasts
26
Where are plasmablasts generated? Where do they home?
GC, enter circulation to home to bone marrow and differentiate into long-lived plasma cells
27
how are plasma cells maintained?
BAFF
28
What % of Ab in the blood is produced by long-lived plasma cells?
50
29
Where are memory cells generated from? what do they express high levels of?
GC for T-dependent Ag Bcl-2
30
Memory cells typically express what kind of Ag receptors and what kind of Ig molecules?
high affinity (mutated) receptors switched isotype molecules
31
What do effective vaccines against microbes and toxins require?
affinity maturation AND memory B cell formation
32
What are conjugate vaccines? what do they more readily induce?
polysaccharides covalently linked to a foreign protein to form a hapten-carrier equivalent high-affinity Abs and memory cells
33
What are TI characteristics?
multivalent, low level isotype switching (IgM), little or no affinity maturation
34
What are TD characteristics?
proteins, lots of isotype switching, allows affinity maturation and secondary responses
35
How do TI Ags become activated with T cell help?
maximal cross-linking of the BCR complex on B cells
36
Where are TI Ab responses initiated?
spleen, bone marrow, peritoneal cavity, and mucosal sites
37
What kind of B cells are especially important for Ab responses to TI ags?
Marginal zone and B-1
38
what do marginal zone b cells mainly respond to? what do they differentiate into after activation?
polysaccharides short-lived plasma cells that secrete IgM
39
Where may TI Ags persist for long periods of time?
surface of marginal zone macrophages in the spleen
40
What do B-1 cells respond to?
TI Ags in the peritoneum and mucosal sites
41
What do TI Ags of polysaccharide nature activate?
complement system via alternate pathway | generate C3d, binds to Ag, recognized by CR2 on B cell
42
what is the dominant Ab class induced by pneumococcal capsular polysaccharide?
IgG2
43
BAFF produced by DCs and macrophages induces synthesis of what? what facilitates this?
AID in Ag-activated B cells activation of TLR on B cells
44
what mediates IgA switching?
TGF-beta
45
what is the major mechanism of host defense against infections by encapsulated bacteria?
humoral immunity
46
what contributes to the generation of natural Ab?
TI Ags
47
most Abs are ______ produced by ______ stimulated by _____
low affinity anti-carb Abs peritoneal B-1 cells Marginal Zone B cells in the spleen
48
Blood group Ags are important for what but not important for what?
imp: blood transfusions and transplantation NOT: host defense
49
what do polysaccharide vaccines induce?
long-lived protective immunity
50
what happens in b cell activation involving PIP3?
BCR --> PIP3 --> B cell activated
51
what is the mechanism of the FcgammaRIIB receptor?
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