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immunology > 15: B cell activation and Ab 2 > Flashcards

15: B cell activation and Ab 2 Flashcards

1
Q

how are u heavy chain made

A

alternative processing of primary RNA Tc for mRNA

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2
Q

what are the two forms of u heavy chain

A

membrane and secreted form

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3
Q

what for of u protein is made by activated B cells ag dependent

A

secreted form

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4
Q

what makes membrane u mRNA

A

resting B cells

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5
Q

what are TP, TM, and Cy for u mRNA

A

tail piece, transmembrane and cytoplasmic segments

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6
Q

exons of Cu gene

A

Cu1, Cu2, Cu3, Cu4

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7
Q

how many CH regions of IgG, A, D

A

3

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8
Q

how many CH regions for IgE and IgM

A

4

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9
Q

what causes class switching

A

Heavy chain switching in TD response

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10
Q

what are the different classes of heavy chains

A

y,a and E

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11
Q

where does isotype switching usually occur and what causes it

A

GC and is driven by TFH cells

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12
Q

isotype switching that might occur in extrafollicular foci

A

driven by Th cells

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13
Q

what part of heavy chain leads to class switching

A

constant regions

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14
Q

what determines Ab specificity

A

variable regions

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15
Q

what doesn’t change in isotype switching

A

Abs specificity because determine by variable and not constant regions

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16
Q

what does the ability of B cells to produce many Abs cause

A

plasticity in humoral immune response

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17
Q

why need various classes of Abs

A

distinct effector fxns and defense against all different types of pathogens

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18
Q

what causes class switching

A

B cells activated by TFH cells with CD40L and cytokine signals

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19
Q

IgM fxn

A

complement activation

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20
Q

IgG is for

A

opsonization, phagocytosis, complement, neonatal immunity

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21
Q

of does IgG do neonatal immunity

A

placental transfer

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22
Q

IgE fxn

A

helminths, mast cell degradatioin

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23
Q

what does mast cell degranulation cause by IgE

A

immediate hypersensitivity

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24
Q

what works with IgE

A

IgG4

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25
Q

what cytokine activates IgE and IgG4

A

IL4

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26
Q

what is IgA for

A

mucosal immunity

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27
Q

what activates IgA

A

TGF-B, April, BAFF

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28
Q

how are TH1 cells related to Class switching

A

when activated, produces IFNy that induces TFH to produce more IFNy that causes IgG

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29
Q

how does TH2 cause class switching

A

IL-4 causes IgE class switching

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30
Q

what Ig is used for intracellular pathogens

A

IgG Abs

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31
Q

what does IgG do

A

block entry microbes, activate complement and cause phagocytosis by macrophages

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32
Q

what does IgE do for helminths elimination

A

eosinophil and mast cell activation

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33
Q

what controls class switching

A

location of B cells and controlled by local cytokines

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34
Q

mucosal B cells cause

A

IgA

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35
Q

what cytokines induce IgA

A

TGF-B and BAFF

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36
Q

where does TGF-B come from

A

T reg, macrophages

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37
Q

BAFF is produced from

A

DCs and Macrophages

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38
Q

what family does BAFF belong to

A

TNF

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39
Q

how does CD 40 contribute to isotype switching

A

works with cytokines

40
Q

what is the enzyme used for isotype switching and affinity maturation

A

activation-inducing deaminase (AID)

41
Q

what induces AID

A

CD40 engagement

42
Q

what happens when CD40 is deficient

A

Ag is dominated by IgM for limited switching

43
Q

what change in IgM mRNA for IgG1

A

loop out deletion of Cu, C delta and Cy3 for only Cy1

44
Q

what controls how Ig mRNA gets rearranged

A

switching sequence before C genes

45
Q

where does class switching recombination occur and how

A

activated B cells by changing Cu gene to CH genes

46
Q

what does CSR precede

A

Germline Tcs

47
Q

what initiates Germline Tc

A

intronic promoters

48
Q

how do germline Tc work

A

open chromatin of S region to make more accessible to recombinase

49
Q

how does CSR make a looped-out deletion

A

goes between two switch regions with repetitive sequences for loop

50
Q

what regulates CSR

A

cytokines

51
Q

how do all immunoglobin isotypes relate

A

similar Ag specificity with different biological properties

52
Q

how does AID work

A

deaminates cytosines in ssDNA to convert C to U

53
Q

what happens after AID creates U

A

Uracil N Glycosylase removes U for apurinic/ apyrimidinic endonuclease (APE1) to create nicks

54
Q

what does the nick by APE1 lead to

A

ds breaks

55
Q

what does affinity maturation cause

A

increased affinity of Abs for Ag

56
Q

where is the only place that affinity maturation occurs

A

TD Ags

57
Q

what causes mutation of IgV genes

A

TFH with CD40/CD40L interactions

58
Q

GC reaction needed because

A

make B cells with high affinity Ag receptors to produce Abs with highest affinity for Ag

59
Q

B cells survive by

A

high affinity Ig that binds FDC presenting Ags

60
Q

how much is affinity increased by changing an AA

A

10 fold

61
Q

how does Ig V gene get mutated

A

point mutations at high rate

62
Q

how many pt mutations of IgV genes

A

1 in 10^3

63
Q

how much higher is mutation rate for V genes than others

A

1000x higher

64
Q

how many VH and VL genes are in each B cell

A

700

65
Q

how many mutations in V region

A

one per cell division

66
Q

due to B cell clones having V mutations, how different are IgGs from each other

A

5% germline for 10aa substitiution

67
Q

where do most V mutations occur and why

A

V regions at Ag binding region to increase affinity

68
Q

which Ig has more mutations

A

IgG

69
Q

what does a B cell to APC FDC result in

A

rescue B cells from apoptosis

70
Q

B cells to TFH result in

A

B cell survival for CD 40 dependent

71
Q

why is GC a B cell graveyard

A

somatic mutation produce B cells without high affinity as well for apoptosis

72
Q

where do B cells go after somatic mutation

A

FDC light zone

73
Q

how does Ag recognition lead to B cell survival

A

induces expression of BCl-2

74
Q

how is B cell survival promoted when when B cell binds Ag

A

once presents Ag for TFH and bind CD40L, signals survival

75
Q

what do B cells inhibit to promote life

A

activate endogenous inhibitors of Fas by BCR to Ag recognition

76
Q

where does FasL come form and what does it induce

A

TFH expresses FasL and it causes apoptosis

77
Q

how do B lymphomas develop

A

B cells in germinal centers

78
Q

what causes B lymphomas

A

chromosomal translocation of various oncogenes in Ig gene

79
Q

what causes the incorporation of oncogenes into Ig genes

A

DNA breaks by hypermutation and isotype switching

80
Q

what diseases do GC contribute to

A

autoimmunity and B cell lymphomas

81
Q

why are GC centers related to Autoimmunity

A

Somatic mutations may produce self-reactive B cell clones

82
Q

what are plasma cells for

A

Ab production

83
Q

what activates plasma cells

A

signals from BCR, CD40, TLR and other cytokine receptors

84
Q

what makes Short lived plasma cells

A

extrafollicular compartment in TI response as well as early TD response by extrafollicular B cell foci

85
Q

where are short lived plasma cells found

A

secondary lymphoid organs and peripheral of non-lymphoid tissue

86
Q

when are Long lived plasma cells made

A

TD response to proteins Ags in Germinal centers

87
Q

what makes Long lived plasma cells

A

BCR and IL21

88
Q

what is the precursor of long lived plasma cells

A

plasmablasts

89
Q

how do plasmablast become long lived plasma cells

A

generated in GC then home to bone marrow for long lived plasma

90
Q

how do immunizations work

A

use a T cell dependent Ag so that 2 to 3 weeks later, Bone marrow produces many Abs

91
Q

what maintains plasma cells and ow

A

BAFF

92
Q

how long can plasma cells secrete Abs

A

months or years after Ag is no longer present

93
Q

what do Abs provide to body

A

immediate protection if Ags encountered later

94
Q

how many Abs in blood are made from long lived plasma cells

A

50%

95
Q

can memory cells become plasma cells

A

yes

96
Q

pathways of B cells

A

pre B to Naive to MZ or follicular B

immunology (10 decks)

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