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Foundations Test 4 > Humoral Immunity > Flashcards

Humoral Immunity Flashcards

1
Q

FAB

A

Made of Vl and Vh regions…binds the antigen

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2
Q

FC

A

Constant region that determines function and binds to macrophages, T cells, etc.

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3
Q

Antibody hinge region and how is entire thing held together

A

Allows flexibility

Disulfide bonds

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4
Q

How many HV regions per chain

A

3

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5
Q

AB vs. T cell antigen binding

A

AB can bind tons of stuff

T cell only proteins

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6
Q

Other region besdies HV

A

Framework…pretty stable

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7
Q

Antigen binding sites composed of

A

HV regons

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8
Q

AB:antigen interaction due to

A

Noncovalent forces…means it is reversible

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9
Q

Which region only in heavy chain?

A

Diversity region

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10
Q

Which region has most functional gene segments?

A

Variable

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11
Q

Combinatorial diversity

A

Random joining of D/J regions (example)…other regions can be brought together as well

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12
Q

Junctional diversity and how it happens

A

RSS brings together junctions…RAG 1 and 2 generate hairpins at region…TdT adds N-nucleotide additions and alters

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13
Q

In absence of TdT

A

Still some antibodies but lack diversity

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14
Q

Absence of Rag 1 and 2

A

No recombination…therefore no B cell formation

Cause of SCID

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15
Q

Allelic exclusion of AB

A

Only one copy of Ig genes are expressed on an individual cell

A heterozygous Ig will only display one specificity on its surface

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16
Q

Alleles for each type of AB

A 
M - M
G - G1-4
D - D 
E - E 
A - A 1-2
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17
Q

Which activate complement via classical pathway?

A

IgG1 -3
IgM

Bind to C1q

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18
Q

Whcih transfer placental

A

IgG

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19
Q

Which bind to marcophage Fc receptors

A

All but IgM, IgD, and IgG2

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20
Q

Which bind mast and basophils

A

IgE

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21
Q

Which are reactive with Staph protein A

A

IgG

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22
Q

Amount of Igs in serum

A

IgG in serum is most
IgM and IgA present
IgD not in serum
Small IgE

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23
Q

Weird structures of Igs and consequences

A

Dimeric IgA - 4 binding sites
Pentameric IgM - 10 binding sites

Increases avidity - binding of entire molecule

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24
Q

2 types of determinants

A

Conformational - need geometry in order to recognize

Linear determinant - may not be able to bind if there is geometry

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25
Q

B cell developmet

A

Stromal cells aid in development
Go through negative selection in the bone marrow (if bind to self, will try to rearrange and if not, then killing)
Activated outside of bone marrow by lymphoid organs by meeting foreign antigen
Give rise to memory and plasma cells in bone marrow and lymphoid tissue

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26
Q

When B cells first secreted, only have

A

IgM and IgD

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27
Q

Important IL for B cell development

A

IL-7 - uses common gamma chain - deficiency leads to SCID

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28
Q

Which chain develops first

A

Heavy chain…will have IgM before IgD

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29
Q

BK

A

Bruton’s tyrosine kinase

Deficiency leads to B cell deficiency

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30
Q

IL-7R

A

Important in expansion of B cells

31
Q

Arrangement of heavy chain

A

D-J first

then V-DJ

32
Q

L-chain arragnement

A

V-J rearranged

33
Q

Receptor editing of B cells

A

If expression in mu chain is to self, will undergo rearrangement of light chain to try to eliminate this effect…if still bind to self, apoptosis

34
Q

If B cell self-binds to soluble self molecule in bone marrow

A

Anergic B cell migrates to peripher y

35
Q

If B-cell binds very low affinity self molecule in bone marrow

A

Clonally ignorant cell migrates to periphery…could still be activated

36
Q

In spleen, if B cell recognizes self

A

Same things as in bone marrow

Will eventually mature if low-affinity (clonal ignorant) or no reaction (mature)

37
Q

3 things AB does

A

Neutralization
Opsonization
Complement Activation

38
Q

Thymus-dependent B cell stimualtion

A

BCR binds antigen and stimulates signaling…antigen taken in with BCR and processed into class 2 MHC…presented to T cell along with CD40 which binds CD40L…causes class switching from IgM to another type

39
Q

CD40/CD40L defieincy

A

Hyper IgM…can’t class switch…susceptible to pyogenic bacteria

40
Q

T-independent stimulation

A

2 options

Polyvalent antigen cross linking AB binds…no class switching

TLR binds a mitogen - no class switching

41
Q

Polysaccharide activation

A

Is T-independent (no IgG and no memory)…by attaching a protein to the polysaccharide, you can generate memory (IgG)

Hib/pneumococcal conjugate vaccines

42
Q

Tfh cells

A

T follicular helper cells

Bind to B cell using CD40L/CD40 interaction and allow proliferation of B cells by producing cytokines

43
Q

Difference between B and T cell viral activation

A

T cells recognize things on the inside
B cells recognize surface of virus

T cells can help B cells recognize linked epitopes even if not identical

44
Q

How do antigens get into lymph node

A

Via dendritic cells via affarent lymphatics

45
Q

B cells enter lymph nodes through

A

HEVs and move through follicles to germinal centers

46
Q

FDCs have what receptors?

A

Fc and complement receptors

FcR and Cr1

47
Q

PLasma cells wil migrate to

A

Bone marrow

48
Q

2 things that happen during maturation of AB response and where does it happen?

A

Somatic hypermutation - mutated genes and expresson of different AA allows variability
Class switch - changes function

Germinal centers

49
Q

IFN-gamma = which Ig and function?

A

IgG - opson, complement, placental

50
Q

IL-4 = which IG and function/

A

IgE, IgG4 - helminths protection and mast cell degranulation

51
Q

TGF-B, APRIL, BAFF = which Ig and function?

A

IgA…mucosal immunity in lungs and gut

52
Q

Class switching

A

Nothing changes except for constant region

Requires AID

53
Q

Somatic hypermutation

A

Select high-affinity antibodies that change affinity (not specificity)

Requires AID

54
Q

As number of responses increases

A

Number of somatic hypermutations increases as well to select for best antibody

55
Q

If AID is lost then,

A

Lower affinity B cells with mostly IgM antibodies

56
Q

IgA function

A

Secreted into the lumen via pIgR receptor…binds to toxins and pathogens…opsonization for destrution

57
Q

Distribution of AB through body

A

IgG and IgM in blood
Dimeric IgA at mucosal
IgE - around the skin …passed to child

58
Q

Antibody toxin neutralization

A

Prevents binding of toxin to cell

59
Q

Antibody virus neutralization

A

Blocks virus bindign to cell membrane

60
Q

Antibody bacteria neutralizatio

A

Block to adhesins of bacteria and prevent association with cell membrane…also complement

61
Q

Antibody - complement

A

IgM and IgG bind to and activate C1q

62
Q

Antibody immune complexes

A

Get cross linking of antibodies and activate complement…C3b binds to pathogen as well…complement receptor CR1 on erythrocytes binds via C3b…takes ot spleen and liver where phagocytic cells destory

63
Q

Free Ig will not

A

Cross-link Fc receptors on macrophages…need to be bound to bacterial surface

64
Q

Eosinophils attack

A

IgG and IgA coated schistosome larva

65
Q

ADCC

A

AB binds on target…NK cell recognizes and induces apoptosis

66
Q

Mast cell degranulation

A

Via IgE…cross-links

67
Q

In secondayr response, what is differnet?

A

IgA and IgG more than IgM…high affinity, high somatic hypermutation

68
Q

If you see more IgM

A

Then probably early in process and maybe the first time infected

69
Q

If mostly IgG,

A

Pathogen is gone or this is not the first time they have seen ti

70
Q

CD40/CD40L def

A

CD40L (x-linked)

Hyper IgM

71
Q

AID def

A

Hyper IgM

72
Q

BAFF and APRIL def

A

No differentiation into Igs in the spleen

73
Q

TACI def

A

common variable immunodeficiency

Foundations Test 4 (12 decks)

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