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IHO Week 1 > Antibodies > Flashcards

Antibodies Flashcards

1
Q

What see in electrophoresis of lymphoma

A

too much antibody - gamma band

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2
Q

Antibody structure

A

3 fragments:
2 identical Fab
1 Fc

Two identical light chains
Two identical heavy chains

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3
Q

Each chain consists of _______ held together by ______

A

domains

s—s bonds

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4
Q

Light chain has ____ variable/constant

Heavy chain “”””

A

Light - 1 variable (VL), 1 constant (CL)

Heavy - 1 variable (VH), 3-4 constant (CH1, CH2, CH3, CH4)

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5
Q

Which domain pushes out

A

CH2 - interact more easily with complement – how ab initiate inflammation (C1q)

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6
Q

IgM structure

A

pentamer held together by J chain

4 CH

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7
Q

IgG structure

A

3 CH

different kinds

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8
Q

IgA structure

A

dimer - j chian

3 CH

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9
Q

IgD structure

A

primary function is membrane bound in naive B cells to mediate B cell receptor signaling
3 CH
tailpieces (bound)

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10
Q

IgE structure

A

4 CH

secreted as a monomer

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11
Q

What define class of antibody

A

5 kinds of H chains (gamma, alpha, mu, epsilon, delta)

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12
Q

L chain types

A

kappa, lambda (only 1 kind in each antibody)

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13
Q

What happens to chains in class switching

A

heavy chain changes (ie mu –> alpha) but L chain (k or L) stays the same during the switch

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14
Q

constant region made up of

A 
of 1 (in L
chains) to 4 (in epsilon and mu) compact, structurally-similar domains called C domains.
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15
Q

variable domain

A

V domains of both the H and L chain (VH and VL) - where antigen binds

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16
Q

Valence

A

number of antigenic determinants (epitopes) an antibody molecule can theoretically bind.

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17
Q

Valence IgG

A

2

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18
Q

Val IgM

A

10

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19
Q

Val IgA

A

4

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20
Q

Val IgD

A

2

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21
Q

Val VL or VH

A

None (need both)

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22
Q

Val Fab

A

1

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23
Q

Isotypes

A 
IgG1, IgG2, IgG3, IgG4
IgA1, IgA2
IgM1, IgM2
IgD
IgE

subclasses
slight differences in amino acid sequences of H chain C regions

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24
Q

Allotypes

A

Minor allelic differences in sequence of Immunoglobulins between individuals
from parents - useful in genetics

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25
Q

Idiotypes

A

Each antibody will have its unique combining region, made up of the CDR amino acids of its L and H chains

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26
Q

Antibodies in human serum (numbers)

A 
IgG: 1000 mg/deciliter (dL =100 mL) (MOST)
IgA: 200 mg/dL
IgM: 100 mg/dL
IgD: 5 mg/dL (usually bound)
IgE: 0.02 mg/dL (LEAST)
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27
Q

IgG

A

the main antibody in blood and tissue fluids. It neutralizes toxins and blood-borne viruses, binds bacteria and facilitates their destruction by activating complement and by binding them to phagocytic cells.

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28
Q

the main antibody in blood and tissue fluids. It neutralizes toxins and blood-borne viruses, binds bacteria and facilitates their destruction by activating complement and by binding them to phagocytic cells.

A

IgG

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29
Q

similar things in the blood as IgG, but its real role is as the dimer form in secretions, where secretory component protects it from proteolysis.

A

IgA

30
Q

IgA

A

similar things in the blood as IgG, but its real role is as the dimer form in secretions, where secretory component protects it from proteolysis.

31
Q

much the same as IgG. It is the first antibody to appear in the serum after
immunization, and it is very efficient at activating complement. It does not get into tissue fluids very efficiently, nor is it bound efficiently by phagocytic cells.

A

IgM

32
Q

IgM

A

much the same as IgG. It is the first antibody to appear in the serum after
immunization, and it is very efficient at activating complement. It does not get into tissue fluids very efficiently, nor is it bound efficiently by phagocytic cells.

33
Q

role in blood, if any, is uncertain; it seems to function mainly as a receptor on naïve B
cells.

A

IgD

34
Q

IgD

A

role in blood, if any, is uncertain; it seems to function mainly as a receptor on naïve B
cells.

35
Q

antibody which causes Type I immunopathology, also called immediate
hypersensitivity or allergy. Its true importance is in resistance to worms and other parasites.

A

IgE

36
Q

IgE

A

antibody which causes Type I immunopathology, also called immediate
hypersensitivity or allergy. Its true importance is in resistance to worms and other parasites.

37
Q

Ag-Ab interaction change in shape

A

When ab bind ag - change in angle between two Fab parts to more Y or T shaped –> bulging of Fc

38
Q

Ab-Ag interaction results

A

binding of phagocytic cells (bind to Fc altered of IgG - not IgM)
C1q binds 2 adjacent Fcs and activated – IgM better at complement

39
Q

IgG does what better than IgM and vice versa

A

IgG - binding to phagocytic cells

IgM - activating complement

40
Q

steps in heavy chain recombination

A 
DJ recombination
VDJ recombination
transcription
splicing
translation
41
Q

immunoglobulin domains

A

two or more β-pleated sheets arranged in opposite directions that are stabilized by one or more disulfide bonds.

42
Q

Which ab isotypes fix complement

A

IgM (and IgG)

43
Q

Which ab isotypes degranulate mast cell/basophil

A

IgE

44
Q

Which ab isotypes lyse bacteria

A

IgM > IgG, IgA

45
Q

Which ab isotypes have antiviral

A

IgM, IgG, IgA (most)

46
Q

which ab isotypes neutralize toxins

A

IgG, IgA

47
Q

Elevated levels IgM indicate

A

recent infection or other exposure to antigen

48
Q

Which ab binds macrophage Fc receptors

A

IgG (not IgM, IgA)

49
Q

Which ab mediates hemolytic disease of newborn

A

IgG (blue baby, Rh mismatch)

50
Q

Where is antibody diversity from

A

Genetic rearrangement of various gene sections for heavy and light chains (VDJ and constant regions)

Variation incorporated at joining sites for various segments of heavy and light chains

Hypermutation in variable regions of heavy/light chains during proliferation of B cells

Mixing/matching heavy/light chains in combinatorial manner (genes are separate)

51
Q

primary RNA transcripts of heavy chains

A

VDJ - combined with constant regions up to end of delta

can make VDJ-m and VDJ-d

52
Q

light chain recombination

A

only have VJ (no D)

Kappa, if not, then lambda

53
Q

The enzymes that do the recombination of antibody and T cell receptor DNA (VDJ recombination)

A

RAG recombinases

54
Q

Syndrome where RAGs are knocked out -

A

Omenn syndrome

Cannot make B or T cells

55
Q

RAG-1/2

A

Catalyze DNA strand breakage and rejoin to form signal and coding joints

56
Q

Tdt

A

add N region nucleotides to the joints between gene segments in the Ig heavy chains and all joints between TCR gene segments

57
Q

HMG

A

Stabilize binding of RAG1/2 to recombination signal sequences, stabilize bend introduced into the 23-bp spacer DNA by the RAG 1/2 proteins

58
Q

Ku proteins

A

Binds DNA coding and signal ends and holds them in protein-DNA complex

59
Q

ARtemis

A

Opens the coding end hairpins

60
Q

Heavy chain VD and DJ points

A

loss of coding nucleotides at joint – TdT adds in non-templated nucleotides = source of variation (and potential cause of non-productive Ab)

Somatic mutation

61
Q

Mature (but not activated) B cells initially express

A

both IgD and IgM (these are B cell receptors)

62
Q

As mature B cells are activated to divide and differentiate by their cognate antigen, they switch from membrane-bound IgD and IgM to

A

secretory IgM

Level of processing mRNA transcripts

63
Q

Class switching to IgG, IgE or IgA happens at what level

A

rearrangements of DNA

64
Q

Variation through somatic hypermutation

A

Recombined V(D)J is hypermutable, each time a B cell divides after antigenic stimulation - there is a good chance of one daughters iwll make a slightly different antibody = affinity maturation

65
Q

How somatic hypermutation works

A

Activation-Induced (Cytidine) Deaminase (AID) converts random cytosines in the CDR gene regions to uracil. So a C:G pair becomes a uracil: guanine mismatch. The uracil bases are excised by the repair enzyme uracil-DNA glycosylase. Error-prone DNA polymerases then fill
in the gap, creating mostly single-base substitution mutations, so at the end of cell division one daughter may be making a different (worse? better?) antibody.

66
Q

What changes/stays same in class switching

A

In all cases, the L chain and the VH domain stays the same but the C region of the H chain changes.

67
Q

How class swtiching happens

A

cell which has put its particular H-chain VDJ combination together with its mu and delta genes goes back to its DNA, does a loop-out of mu and delta, and puts VDJ next to the C region gene of gamma or epsilon or alpha, while excising and discarding intervening DNA.

require T cell help, AID

68
Q

if a cell makes IgM, what can it make> What about igG

A

IgM –> anything else (still have DNA)

IgG cannot go back to make IgM since mu info is gone (from the DNA)

69
Q

IL2, IL4, IL5

A

B cell proliferation

70
Q

B cell proliferation

A

IL2, IL4, IL5

71
Q

IL4 + IL5

A

B cell class switch to IgE

72
Q

IFN gamma

A

block class switch to IgE induced by IL-4

IHO Week 1 (9 decks)

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