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Infection and immunity > 5. Humoral responses > Flashcards

5. Humoral responses Flashcards

1
Q

what cells are involved in the humoral response

A

B cells and antibodies

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2
Q

where do b cells develop and mature?

A

the bone marrow

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3
Q

what is the b cell receptor?

A

a surface immunoglobulin with a transmembrane region and attached to a signalling domain
the same Ig the b cell will secrete

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4
Q

when b cells first encounter the antigen what is phosphorylated?

A

Src family kinases to activate downstream signallinig pathways

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5
Q

how does a b cells change in morphology once activated?

A

a bigger nucleus for replication
proteins and machinery to make antibodies

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6
Q

general antibody structure

A

2 identical light chains
2 identical heavy chains
linked with a disulphide bond

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7
Q

where does papain cleave antibodies?

A

above the disulphide bond leaving 2 FAB fragments and 1 Fc region

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8
Q

where does pepsin cleave antibodies?

A

below the disulphide bond leaving 1 FAB fragment and 1 Fc fragment

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9
Q

what does each light chain consist of?

A

one variable region
one constant region

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10
Q

What does each heavy chain consist of?

A

one varible region
multiple constant region domains

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11
Q

what is the function of the hinge region ?

A

allows flexibility when binding to multiple antigens

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12
Q

what are the hypervariable regions?

A

exposed loops on the outside of the antibody that bind to antigens
they are hypervariable to bind to a diverse range of antigens

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13
Q

What are the framework regions?

A

a series of B sheets to provide structural integrity to the antibody and keep the variable regions in place

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14
Q

where are the 3 hypervariable regions encoded?

A

on a single v-region exon

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15
Q

how do we generate a diverse range of antibodies?

A

somatic recombination of seperate gene segments

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16
Q

what gene segments do light chains have?

A

variable and joining and a constant region

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17
Q

what gene segments do heavy chains have?

A

variable, diversity and joining and 1 of 5 constant regions

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18
Q

what is the leader peptide?

A

a signal sequence that directs the Ig to secretory pathways

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19
Q

what are the 2 light chain gene loci?

A

lambda and kappa
only 1 is used in each antibody

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20
Q

what heavy chains can light chains combine with?

A

any heavy chain

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21
Q

what flanks each gene segment?

A

Recombination signal sequences (RSS)

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22
Q

why are RSSs highly conserved?

A

they prevent rearrangment with the same cluster
eg a j cant join to a j
v cant join to v

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23
Q

what is the 12/23 rule with signal sequences?

A

a 23 RSS can only bind with a 12 RSS
prevents joining of different segments of the same type and ensures D region is included in heavy chain recombination

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24
Q

what enzymes are in the VDJ recombinase enzyme complex?

A

Lymphocyte specific RAG-1 and RAG-2 endonuclease
Artemis:DNA-PK
DNA ligase 4

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25
Q

what do RAG1 and RAG2 do?

A

binds to an RSS region and recruit another RSS region to it
then cleaves and loops out the DNA between the 2 RSSs

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26
Q

Artemis:DNA-PK does what in double-stranded break repair?

A

opens the hair pin formed during cleavage

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27
Q

what does terminal deoxynucleotide transferase do in double-strand break repair?

A

randomly adds nucleotides to the gap

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28
Q

what does DNA ligase do in double-strand break repair?

A

joins the new DNA backbone together making a continuous piece of DNA

29
Q

how do B cells generate diversity?

A

combinatorial diversity
junctional diversity
somatic hypermutation

30
Q

what is combinatorial diversity?

A

differnet VDJ combinations
different heavy chain light chain combination

31
Q

what is junctional diversity?

A

imprecise addition and removal of nucleotides in recombination

32
Q

what needs to happen for somatic hypermutation?

A

encountering the antigen
CD4 T cells

33
Q

what does somatic hypermutation do?

A

Increases the mutation rate in the antibodies to make variable regions fit the antigen better

34
Q

what enzyme initiates the hypermutations?

A

Activation-induced cytidine deaminase (AID)

35
Q

what is affinity maturation ?

A

selects for the survival of the antibodies that have the highest affinity for the antigen

36
Q

what is a disadvantage of hypermutation?

A

some mutations can be detrimental and prevent function
these b cells are apoptosed

37
Q

how are the affinity matured cells selected?

A

the b cells with the better antigen presentation as a result of antigen binding receive enhanced survival signals from CD4 T cells

38
Q

what secondary signal is needed for activation in a thymus dependent antigen?

A

the CD40 receptor and MHC2 on the B cell binding to a CD40L and TCR on a CD4 helper cell
(1st signal is BCR binding)

39
Q

what secondary signal is needed for activation in a thymus independent antigen?

A

binding of a common microbial part to a TLR
(1st signal is BCR binding)

40
Q

what determines antibody effector function?

A

the Fc portion

41
Q

what functions do antibodies have?

A

neutralisation
opsonisation
antibody mediated cellular cytotoxicity
trigger mast cell activation
activation of complement

42
Q

where does class switching occur?

A

at the genome level

43
Q

where are the Fc genes located?

A

downstream of the VDJ regions

44
Q

what is IgA functions?

A

secreted across mucosal membrane

45
Q

IgM

A

Pentamer
early in response
no hypermutation so more binding sites

46
Q

As IgM and IgD are derived on the same pre-mRNA transcript what determines which is expressed?

A

alternative splicing of the mRNA and polyadenylation

47
Q

What does AID do?

A

cuts out switch regions at the 5’ end to loop out other heavy chain genes

48
Q

what process is AID involved in?

A

Class-switching and Double-strand break repair mechanisms

49
Q

what does an AID deficiency result in?

A

No ability to class switch or affinity mature
Leads to Hyper IgM type 2 immunodeficiency

50
Q

what is the dynamics of the different antibodies in the immune response?

A

Initially IgM dominates and then as affinity maturation occurs IgG dominates
somatic hypermutation means affinity increases

51
Q

what determines which class the antibody switches to?

A

the cytokines secreted by T helper cells

52
Q

Which antibodies are stimulated by IL-4?

A

IgE and IgG1

53
Q

Which antibodies are stimulated by IFNy?

A

IgG3 and IgG2a

54
Q

Which antibodies are stimulated by TGFb?

A

IgA and IgG2b

55
Q

Which antibodies are stimulated by IL-21?

A

IgA, IgG3 and IgG1

56
Q

Which antibodies are stimulated by IL-5?

A

IgA and IgG1

57
Q

where do you find IgG and IgM?

A

in the circulation

58
Q

where do you find IgA?

A

in mucosal sites like GI tract and Respiratory tract
also breast milk

59
Q

where do you find IgE?

A

directly under the skin
in mouth and nose
lining external surfaces

60
Q

what is antibody neutralisation?

A

bind to viruses, bacteria and toxins to prevent interaction with receptors in the cells

61
Q

what antibodies mainly carry out neutralisation?

A

IgG and IgA

62
Q

what is antibody opsonisation?

A

Coating the bacteria with the antibodies and then binding to the pathogen surfaces to trigger phagocytosis by crosslinking Fc receptors

63
Q

what antibodies carry out opsonisation?

A

IgA, IgG1, IgG3 and IgG4

64
Q

what does IgE opsonisation look like?

A

binding to parasites and eosinophils Fc receptors crosslinking to trigger degranulation

65
Q

what is Antibody-dependant cellular cytotoxicity?

A

Recognising Viral proteins on host cells and bind Fc receptors on NK cells
crosslinking of NK cell Fc receptors causes degranulation and killing of host cells

66
Q

what antibodies are involved in Antibody-dependant cellular cytotoxicity?

A

IgG1 and IgG3

67
Q

what is antibody sensitisation of mast cells?

A

cross-linking of IgE triggers degranulation and inflammatory mediators like histamine
allergy response

68
Q

how do antibodies activate the complement cascade?

A

IgM or IgG binding to the antigen
C1q then binds to multiple IgG or 1 IgM which can then produce a C3 convertase

Infection and immunity (22 decks)

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