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
B cell developmet
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
26
When B cells first secreted, only have
IgM and IgD
27
Important IL for B cell development
IL-7 - uses common gamma chain - deficiency leads to SCID
28
Which chain develops first
Heavy chain...will have IgM before IgD
29
BK
Bruton's tyrosine kinase | Deficiency leads to B cell deficiency
30
IL-7R
Important in expansion of B cells
31
Arrangement of heavy chain
D-J first | then V-DJ
32
L-chain arragnement
V-J rearranged
33
Receptor editing of B cells
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
If B cell self-binds to soluble self molecule in bone marrow
Anergic B cell migrates to peripher y
35
If B-cell binds very low affinity self molecule in bone marrow
Clonally ignorant cell migrates to periphery...could still be activated
36
In spleen, if B cell recognizes self
Same things as in bone marrow Will eventually mature if low-affinity (clonal ignorant) or no reaction (mature)
37
3 things AB does
Neutralization Opsonization Complement Activation
38
Thymus-dependent B cell stimualtion
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
CD40/CD40L defieincy
Hyper IgM...can't class switch...susceptible to pyogenic bacteria
40
T-independent stimulation
2 options Polyvalent antigen cross linking AB binds...no class switching TLR binds a mitogen - no class switching
41
Polysaccharide activation
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
Tfh cells
T follicular helper cells | Bind to B cell using CD40L/CD40 interaction and allow proliferation of B cells by producing cytokines
43
Difference between B and T cell viral activation
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
How do antigens get into lymph node
Via dendritic cells via affarent lymphatics
45
B cells enter lymph nodes through
HEVs and move through follicles to germinal centers
46
FDCs have what receptors?
Fc and complement receptors | FcR and Cr1
47
PLasma cells wil migrate to
Bone marrow
48
2 things that happen during maturation of AB response and where does it happen?
Somatic hypermutation - mutated genes and expresson of different AA allows variability Class switch - changes function Germinal centers
49
IFN-gamma = which Ig and function?
IgG - opson, complement, placental
50
IL-4 = which IG and function/
IgE, IgG4 - helminths protection and mast cell degranulation
51
TGF-B, APRIL, BAFF = which Ig and function?
IgA...mucosal immunity in lungs and gut
52
Class switching
Nothing changes except for constant region Requires AID
53
Somatic hypermutation
Select high-affinity antibodies that change affinity (not specificity) Requires AID
54
As number of responses increases
Number of somatic hypermutations increases as well to select for best antibody
55
If AID is lost then,
Lower affinity B cells with mostly IgM antibodies
56
IgA function
Secreted into the lumen via pIgR receptor...binds to toxins and pathogens...opsonization for destrution
57
Distribution of AB through body
IgG and IgM in blood Dimeric IgA at mucosal IgE - around the skin ...passed to child
58
Antibody toxin neutralization
Prevents binding of toxin to cell
59
Antibody virus neutralization
Blocks virus bindign to cell membrane
60
Antibody bacteria neutralizatio
Block to adhesins of bacteria and prevent association with cell membrane...also complement
61
Antibody - complement
IgM and IgG bind to and activate C1q
62
Antibody immune complexes
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
Free Ig will not
Cross-link Fc receptors on macrophages...need to be bound to bacterial surface
64
Eosinophils attack
IgG and IgA coated schistosome larva
65
ADCC
AB binds on target...NK cell recognizes and induces apoptosis
66
Mast cell degranulation
Via IgE...cross-links
67
In secondayr response, what is differnet?
IgA and IgG more than IgM...high affinity, high somatic hypermutation
68
If you see more IgM
Then probably early in process and maybe the first time infected
69
If mostly IgG,
Pathogen is gone or this is not the first time they have seen ti
70
CD40/CD40L def
CD40L (x-linked) Hyper IgM
71
AID def
Hyper IgM
72
BAFF and APRIL def
No differentiation into Igs in the spleen
73
TACI def
common variable immunodeficiency