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Microbiology BDS1 > Adaptive Immunity 2 > Flashcards

Adaptive Immunity 2 Flashcards

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1
Q

what do B cells communicate with?

A

T cells

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2
Q

what do B cells produce?

A

antibodies

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3
Q

what does clonal expansion lead to?

A

generation of two subsets

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4
Q

what are plasma cells?

A

great big antibody factories

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5
Q

why are memory B cells important?

A

to mount a quicker antibody response to any subsequent infections

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6
Q

where do B cells mature?

A

in the bone marrow

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7
Q

where are B cells found?

A

they circulate in the blood and lymph and are found in large numbers in lymphoid organs

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8
Q

how do B cells recognise antigens?

A

through B cell receptor (BCR) which is the actual antibody (IgM or IgD)

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9
Q

what does diversity in BCR mean?

A

potential to respond to numerous antigens

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10
Q

once B cells are activated what do they change into?

A

plasma cells (antibody factories)

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11
Q

what are the three main receptors of adaptive immunity?

A

T cell receptor, B cell receptor and MHC

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12
Q

what does multiple genes encoding allow?

A

the development of a repertoire of receptors with wide specificity

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13
Q

which immunoglobulins can be B cell receptors?

A

IgM or IgD

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14
Q

what are the five different immunoglobulins produced by B cells

A

IgG, IgE, IgD, IgM and IgA

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15
Q

what is the most prominent antibody in the human body?

A

IgG

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16
Q

how many subsets can IgG be divided into?

A

4

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17
Q

how many subsets can IgA be divided into?

A

2

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18
Q

what is IgM capable of doing?

A

binding multiple antigens

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19
Q

what are the regions of B cell receptors?

A

constant and variable

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20
Q

what are the chains that B cell antibodies have?

A

light and heavy chains

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21
Q

what are the three main functions for antibodies in the human body?

A

neutralisation, opsonisation and initiation of complement

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22
Q

what is the primary goal of antibodies?

A

to prevent microbial activity and aid removal of threat from host

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23
Q

what is opsonisation?

A

the coating of pathogens by antibodies or complement proteins

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24
Q

what can opsonisation of pathogens by antibodies lead to?

A

phagocytosis, antibody dependent cellular cytotoxicity, mast cell degranulation

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25
Q

what complement pathway do antibodies initiate?

A

classical

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26
Q

what is the steps of antibody depended cellular cytotoxicity?

A

antibodies bind antigens on the surface of target cells, NK cell CD16 Fc receptors recognise cell-bound antibodies, cross-linking of CD16 triggers degranulation into a lytic synapse, tumour cells die by apoptosis

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27
Q

which antibodies give the greatest response in the classical pathway?

A

IgG and IgM

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28
Q

what is each B cell development stage defined by?

A

rearrangements of the immunoglobulin heavy and light chain genes

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29
Q

where do B cells go once they are in the periphery?

A

they migrate to secondary lymphoid organs

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30
Q

what does B cell development generate?

A

diversity

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31
Q

what are the steps of B cell development from being a stem cell?

A

stem cell - lymphoid progenitor - pro-B cell - early pre-B cell - late pre-B cell - immture B cell - mature B cell - either plasma cell OR memory B cell

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32
Q

what must the B cell be to be in the periphery?

A

mature

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33
Q

what genes does the heavy chain involve?

A

V, D, J

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34
Q

what genes does the light chain involve?

A

V and J

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35
Q

what is the main immature B cell receptor?

A

IgM

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36
Q

what receptors do mature B cells express?

A

IgM and IgD

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37
Q

where are IgM and IgD found on mature B cells?

A

the surface

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38
Q

what type of selection do B cells go and whereabouts?

A

negative selection in the bone marrow

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39
Q

what happens to self-reacting B cells?

A

macrophages engulf and remove them

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40
Q

what does selection ensure?

A

that there is no reactivity against self antigens

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41
Q

what are the major functions of antibody?

A

prevention of microbial adhesion, activation of complement, neutralisation of toxin, opsonisation to promote phagocytosis

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42
Q

what does diversity of antibody specificity involve?

A

gene-rearrangements during development

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43
Q

what type of B cells are antigen naive?

A

mature B cells

44
Q

what are the two types of B cell activation?

A

thymus-depended antigens and thymus-independent antigens

45
Q

what are thymus-dependent antigens?

A

antigens which require T cell help

46
Q

what are thymus-independent antigens?

A

antigens which don’t require T cell help

47
Q

where does B cell activation occur?

A

lymph nodes

48
Q

what does activation of naive B cells result in?

A

the rise of plasma cells

49
Q

how many signals are required for thymus independent antigen activation?

A

1 (antigen directly attach to B cell receptors leading to downstream signalling) but a second may exist

50
Q

how many signals are required for thymus dependent antigen activation?

A

2 (co-stimulatory molecules on T helper cells and cytokines)

51
Q

what does T cell and BCR interactions require?

A

co-receptor binding (CD40 to CD40L)

52
Q

what do cytokine signals released from T helper cells induce?

A

proliferation

53
Q

what does antigen dependent B cell activation generate?

A

a pool of plasma cells which produce antibody and memory B cells

54
Q

what do plasma cells initially produce?

A

IgM

55
Q

what antibody is produced by plasma cells once class-switched from IgM?

A

IgG

56
Q

with the antigen independent B cell activation is antibody response stronger or weaker than antigen depended B cell activation?

A

weaker

57
Q

what does antigen independent B cell activation NOT lead to?

A

generation of memory B cells (no long term immunity)

58
Q

what does the activation of B cells lead to?

A

class switching

59
Q

why does class switching take place?

A

because IgM response is weak

60
Q

how does class switching occur?

A

by gene rearrangement but antigen binding site remains the same

61
Q

what does repeated exposure to antigen cause?

A

affinity maturation - the antibody has increasing affinity for antigen

62
Q

what does affinity mean?

A

strength of binding of single antibody to antigen

63
Q

what does avidity mean?

A

ability of antibodies to form complexes

64
Q

what antibody is bivalent?

A

IgG

65
Q

what antibody is decavalent?

A

IgM

66
Q

with regards to IgM, what is its affinity and avidity?

A

low affinity and high avidity

67
Q

what does avidity give and what does it take into account?

A

it gives a measure of the overall strength of an antibody-antigen complex and takes into account valency of an antibody-antigen interaction

68
Q

what is valency?

A

the amount of antigen binding sites

69
Q

what are the characteristics of IgG?

A

highest opsonisation and neutralisation activities, classified into four subclasses (IgG1, IgG2, IgG3, IgG4)

70
Q

what are the characteristics of IgM?

A

produced first upon antigen invasion, increases transiently

71
Q

what are the characteristics of IgA?

A

expressed in mucosal issues, forms dimers after secretion

72
Q

what is the characteristics of IgD?

A

unknown function

73
Q

what is the characteristics of IgE?

A

involved in allergy

74
Q

where is IgA secreted?

A

oral cavity, oesophagus and small intestine

75
Q

what does cross talk between B and T cells lead to?

A

generation of both arms of the adaptive immune response

76
Q

what are both the arms of the adaptive immune response?

A

humoral and cellular immunity

77
Q

what are germinal centres?

A

hubs for T cell and B cell cross talk and proliferation and differentiation, and somatic hypermutation

78
Q

what is somatic hypermutation?

A

the response of an immune cell to external stimuli from an antigen

79
Q

what does antigen exposure lead to?

A

immunological memory

80
Q

what does the presence of memory T and B cells mean?

A

that upon second exposure the immune system can respond much faster

81
Q

what antibody produces a more effective response immediately?

A

IgG

82
Q

summarise the basic principle of vaccination

A

B and T cells, antigen exposure leads to immunological memory, memory B and T cells ensure a faster response on second exposure, primed cells produce a more effective IgG response immediately

83
Q

what does the higher antigen affinity of IgG mean?

A

the secondary response is much more specific

84
Q

what is immune tolerance?

A

the immune system can become dysfunctional and in a state of immune unresponsiveness to a particular antigen or set of antigens

85
Q

what is immunological tolerance?

A

an active response to a particular antigen and it can happen in B and T cells

86
Q

what are the two main types of tolerance?

A

central and peripheral

87
Q

where does central tolerance occur?

A

in the primary lymphoid organs (thymus and bone marrow)

88
Q

where does peripheral tolerance occur?

A

outwith the thymus and bone marrow

89
Q

what are immunogens?

A

antigens that elicit immune responses

90
Q

what do tolerogens induce?

A

an unresponsive state

91
Q

what are the two types of central tolerance selection for T cells?

A

positive and negative

92
Q

what does selection lead to?

A

the elimination of >90% of T cells

93
Q

where does T cell selection occur?

A

in the thymus

94
Q

what is the type of selection for B cells?

A

negative selection - B cells that bind strongly to self antigen are eliminated

95
Q

where does B cell selection occur?

A

bone marrow

96
Q

what does it mean if some tolerance mechanisms are dysfunctional?

A

autoimmunity/allergies

97
Q

what is peripheral tolerance?

A

not all self-reactive T cells are eliminated however, peripheral tolerance prevents their activation

98
Q

what does signal 1 but no signal 2 result in?

A

anergy

99
Q

what does signal 1 and 2 but no signal 3 result in?

A

deletion by apoptosis

100
Q

how can T regualtory cells directly block activity?

A

by binding antigen (both self and foreign antigen)

101
Q

where does peripheral tolerance occur?

A

in the lymphoid organs

102
Q

why do self reactive B cells become anergic in peripheral tolerance?

A

because most self-reactive T cells are eliminated and B cells do not receive T cell help

103
Q

how do T cells help activate B cells?

A

antigen recognition induces expression of effector molecules by the T cell which activates the B cell

104
Q

what does a breach of tolerance to self antigens or commensal organisms drive?

A

many autoimmune diseases

105
Q

what does tolerance ensure?

A

the immune system does not attack slef antigens

106
Q

why are central and peripheral tolerance checkpoints in place?

A

to prevent autoimmunity

Microbiology BDS1 (20 decks)

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