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immunology > partridge > Flashcards

partridge Flashcards

1
Q

what are the 3 main functions of the immune system

A
  1. protects against infectious disease
  2. distinguishes between self and non self
  3. can recognise “danger signals” from cells and tissues
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2
Q

what are bacteria that are generally friendly that inhabit our organism referred to?

A

commensal

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3
Q

what are bacteria that take advantage of an opportunity not normally available such as a host with a weakened immune system called

A

opportunistic

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4
Q

what can the immune system cause if inappropriately activated

A

disease

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5
Q

if the immune system is no longer tolerant of our own cells it can lead to autoimmune diseases such as

A

SLE

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6
Q

what are allergies caused by

A

inappropriate response of immune system against something innocuous in the environment

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7
Q

what is passive immunisation

A

administration of immune components from an immunised source

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8
Q

what is the main difference between active immunisation and passive immunisation

A

ctive immunity involves the body producing antibodies in a response to a pathogen whereas passive immunity involves antibodies obtained from outside the body

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9
Q

which is the oldest form of immunity innate/adaptive

A

innate

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10
Q

which form of immunity is highly specific

A

adaptive

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11
Q

which form of immunity posseses a memory meaning resistance is improved by repeat infection

A

adaptive

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12
Q

which form of immunity produces the fastest response

A

innate

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13
Q

what are the leuocytes in innate immunity

A

phagocytes and NK cells

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14
Q

what are the leuocytes in adaptive immunity

A

B and T lymphocytes

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15
Q

name 5 key components of innate immunity

A 
lysozyme
complement 
interferons
NK cells
phagocytes
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16
Q

what is the soluble factor in adaptive immunity

A

antibodies

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17
Q

what are all haemopoetic cells derived from

A

pluripotent cells

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18
Q

what 2 main cell lineages do haemopoetic cells mainly give rise to

A

myeloid

lymphoid

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19
Q

what do myeloid cells give rise to

A 
nitrophils
dendrites
basophil
mast cells
monocytes
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20
Q

what do lymphoid cells give rise to

A

NK cells

B and T lymphocytes

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21
Q

where are neutrophils present

A

in blood

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22
Q

what do the granules in neutrophils function as

A

specialised lysosomes - release enzymes to deal with bacteria

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23
Q

are neutrophils short or long lived

A

short

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24
Q

where are mononuclear phagocytes generated and present

A

bone marrow and present in blood

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25
Q

what do mononuclear phagocytes differentiate into in tissues

A

macrophage

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26
Q

what do macrophages do

A

help initiate adpative responses

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27
Q

what do monocyes/macrophages/mast cells act as

A

sentinel cells

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28
Q

what do sentinel cells do

A

look out for danger and signal when its present

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29
Q

what do the big granules in mast cells release

A

inflammatory mediators

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30
Q

what do mast cells express high affinity receptors for

A

IgE

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31
Q

what are dendritic cells specialised in

A

presenting antigrn to T cells

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32
Q

what is the name of a type of lymphocyte that can deal with viral infections

A

NK cell

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33
Q

what do the receptors on NK cells recognise

A

altered self

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34
Q

what do phagocytes and other myeloid cells posses to recognise pathogens

A

PRRs on them recognise PAMPS on pathogen

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35
Q

what doe PRR stand for

A

pattern recognition receptor

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36
Q

what does PAMP stand for

A

pathogen associated molecular pattern

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37
Q

where do B lymphocytes mature

A

bone marrow

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38
Q

where do T lymphocytes mature

A

thymus

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39
Q

what is the receptor for B cell lymphocytes

A

antigen

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40
Q

what receptor does a T cell have

A

T cell receptor

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41
Q

how does a B lymphocyte respond to infection

A

secrete antibody

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42
Q

how does a T lymphocyte respond to infection

A

kills infected host cells and makes cytokines

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43
Q

what type of immunity includes B lymphocytes

A

humoral

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44
Q

what type of immunity includes T lymphocytes

A

cell mediated

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45
Q

when a receptor recognises a molecule what happens to the B/T lymphocyte

A

it differentiates further

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46
Q

what is IgG important in

A

secondary responses

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47
Q

what is IgM important in

A

primary responses

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48
Q

what does IgA do

A

protects mucosal surfaces

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49
Q

what is IgE involved in

A

allergy and protection against large parasites

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50
Q

what are the 2 major classes of T lymphocytes

A

T helper cells

T cytotoxic cells

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51
Q

what are T helper cells positive for

A

CD4

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52
Q

what are T cytotoxic cells positive for

A

CD8

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53
Q

which T lymphocytes help B cells make antibody and activate macrophages and NK cells

A

T helper

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54
Q

which T cells recognise and kill infected host cells

A

T cytotoxic

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55
Q

what are cytokines

A

small secreted proteins involved in the communication between cells of the immune system

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56
Q

what are the 3 major groups of cytokines

A

interleukins, interferons and chemokines

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57
Q

what are chemokines involved in

A

cell movement or chemotaxis

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58
Q

all organisms have an innate immunity true/false

A

true

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59
Q

why is innate immunity particularly important in young children

A

used in period between loss of maternal antibodies and formation of own

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60
Q

what does the innate response have a crucial role in initiating and directing

A

adaptive immune response

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61
Q

why is the innate response particularly vital in tackling organisms that mutate quickly

A

adaptive immunity has a lag of 4-6 days. delay may have problems

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62
Q

which type of immunity is complement present in

A

both innate and adaptive

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63
Q

how does complement kill a microbe

A

complement proteins form holes in the bacterial membranes

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64
Q

how does complement cause amplification

A

by activation cascade

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65
Q

what is the classical pathway complement

A

C1 , 4, 2, 3, 5, 6, 7, 8, 9

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66
Q

what is the classical pathway of complement activation important in

A

the adaptive response

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67
Q

what is the most abundant component of complement

A

C3

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68
Q

what are many activated complement components

A

serine proteases

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69
Q

what is C3 cleaved into when cleaved by a C3 convertase

A

C3b + C3a

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70
Q

which is largest the fragment - C3a or C3b

A

C3b

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71
Q

what does cleavage of C3 expose which can then bind to the pathogen through hydroxyl or amie linkages on surface of pathogen

A

thioester in C3b

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72
Q

there are 3 main pathways of complement activation. what do they all generate

A

C3 convertase

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73
Q

what are the 3 pathways of complement activation

A
  1. classical pathway
  2. mannose-binding lectin pathway
  3. alternative pathway
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74
Q

how does the classical pathway gernerate a C3 convertase

A 
antibody bound to molecule
C1q binds anitbody
causes conformational change in C1r,s
turns into protease which cleaves C2 and C4
these combine to make C3 convertase
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75
Q

wat does the classical pathway of complement activation require

A

antibody

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76
Q

what is lectin

A

a molecule that binds to carbohydrates

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77
Q

what is commonly found on the surface of pathogens that mannose binding lectin binds to

A

mannose

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78
Q

how does MBL pathway generate C3 convertase

A

lectin binds mannose on surface of pathogen
complex then activates MASP1 and MASP2
these cleave C4 and C2 which form C3 convertase

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79
Q

for the classical and MBL pathway what C3 convertase is used

A

C4bC2a

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80
Q

how is the C3 convertase generated in the alternative pathway

A 
some C3b is generated spontaneously
C3b binds to pathogen surface
Factor B binds
Factor D cleaves factor B
forms C3 convertase C3Bb
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81
Q

how can you get amplification in alternative pathway

A

C3b generated by classical or MBL pathway can also bind factor B

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82
Q

after generation of C3 convertase allthe pathways of complement activation are the same. true/false

A

true

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83
Q

what are the steps of complement activation after C3 convertase is generated

A

C3 convertase with C3b generates C5 convertase
C5 convertase cleaves C5 into C5a and C5b
C5b activates membrane attack complex that forms pore in outer membrane

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84
Q

what are the 3 main biological activities that complement causes i

A

opsonisation
activation of immune syste
lysis of foreign cells

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85
Q

how does opsonisation occur

A

neutrophils have receptors for C3b - so can recognise pathogen better after complement activation

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86
Q

how does complement activation activate the immune system

A

C5a and C3a are anaphylatoxins - stimulate degranulation of vasoactive factors from mast cells/phagocytes
they also stimulate chemotaxis

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87
Q

how does complement cause lysis

A

active membrane attack complex forms pore in bacterial outer membrane

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88
Q

why does complement need to be regulated

A

when activated it can cause damage

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89
Q

what are 4 examples of complement regulatory proteins

A

factor H
C1 inhibitor
carboxypeptidase N
C59

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90
Q

what does factor H compete with

A

factor B in C3b binding

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91
Q

what does carboxypeptidase N inactivate

A

C3a and C5a

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92
Q

what does C59 bind to prevent MAC formation

A

C9

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93
Q

what can deficiencies in inhibitors of complement such as factor H cause

A

age related macular degeneration

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94
Q

what are cells that are the frontline of response such as mast cells and tissue macrophages called

A

sentinel cells

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95
Q

what are receptors of the innate immune system encoded through

A

germline genes

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96
Q

what are the receptors of the adaptive immune syste assembled during

A

lymphocyte development

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97
Q

what receptors play a key role in innate immunity

A

PRR (pathogen recognition receptors)

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98
Q

what do PRR’s recognise

A

PAMPS (pathogen associated molecular patterns)

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99
Q

what are DAMPS and what is their purpose

A

damage associated molecular patterns. signal when a cell is damaged

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100
Q

what are some examples of DAMPS

A
  • feagments of extracellular matrix
  • posphotidylserine on surface
  • heat shock proteins
  • mitochondrial components
  • build up of purines
  • DNA ouutside of cell
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101
Q

what are 2 examples of soluble pattern recognition receptors

A

mannose binding lectin

complement

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102
Q

what are 4 examples of membrane pathogen recognition receptors

A

lectin receptors
scavenger receptors
chemotactic receptors
toll like receptors

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103
Q

what is one example of a cytoplasmic pathogen recognition receptor

A

NOD receptors

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104
Q

what do chemotactic receptors recognise

A

chemoattractants

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105
Q

what does chemoattractants do

A

guide phagocyte to site of infection and increase the efficiency of intracellular killing

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106
Q

where were toll like receptors identified

A

drosophila

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107
Q

where are toll like receptors found

A

cell surface or endosomes

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108
Q

what does binding of PAMP to a toll like receptor induce

A

expression of cytokines

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109
Q

name two cyotplasmic receptors

A

NOD like receptors (NLR)

RIG-I like receptors

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110
Q

what do NOD like receptors signal the expression of

A

pro inflammatory cytokines

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111
Q

what do RIG-like receptors signal the expression of

A

interferons

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112
Q

inflammation occurs when cells recognise a pathogen and send out signals to other …… …..

A

immune cells

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113
Q

what can chronic inflammation eventually cause

A

many diseases and conditions (cancers and rheumatoid arthritis)

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114
Q

what are the 4 signs of inflammation

A

redness, swelling, heat and pain

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115
Q

release of what causes inflammation

A

inflamatory mediators

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116
Q

dilation of what causes inflammation

A

arterioles, venules and capillaries

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117
Q

increased permeability and blood flow is a cause of inflammation. true/false

A

true

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118
Q

what cells migrate to inflammatory focus in inflammation

A

immune cells

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119
Q

name some inflammatory mediators

A 
prostaglandins
cytokines
chemoattractants
complement proteins
vasoactive amines (histamine)
clotting factors
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120
Q

wha is extravasation

A

movement of leukocytes from blood into tissues

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121
Q

what are the steps to extravasation

A
  1. cytokines in the infected tissue induce endothelial cells to express adhesion moleules such as selectins
  2. neutrophils are captures by selectins which causes them to slow and roll along vessel wall
    3 leukocytes express integrins which are important in cell adhesion. these bind to adhesion molecules on the endothelial cells
  3. stimulates retraction of endothelium cells so neutrophils can move into tissues by chemotaxis
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122
Q

name the adhesion molecules on endothelial cells that are important in extravasation

A

ICAM-1 and VCAM-1

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123
Q

which type of inflammation can be damaging

A

chronic

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124
Q

what does autocrine mean

A

cytokines (hormones) that act in same cell they are expressed

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125
Q

what does paracrine mean

A

cytokines (hormones) that are produced by one type of cell, act on other cells locally

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126
Q

what does endocrine mean

A

cytokines (hormones) that can have an effect on distant cells from where they are produced

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127
Q

cytokines can be described as pleiotropic, what does this mean

A

can have different effects on different cells

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128
Q

cytokines can be grouped into families based on what

A

their structure

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129
Q

the IL-1 family of cytokines need cleaving by what for activation

A

inflammasome

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130
Q

what does the haematopoietin superfamily off cytokines include

A

factors involved in cell growth and differentiation in bone marrow (IL-2, IL-4, IL-6)

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131
Q

what do the interferons family of cytokines interfere with

A

viral replication

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132
Q

what are the majority of TNF family of cytokines

A

transmembrane proteins but can be released in soluble form following cleavage

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133
Q

what are chemokines involved in

A

cell movement

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134
Q

chemokine receptors are which type

A

G protein coupled receptors

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135
Q

what is the main receptor of TNFα

A

TNFR1

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136
Q

TNFα forms….

A

trimers

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137
Q

TNFα can activate 2 pathways, these are

A

cell stimulation

activation of cascases and apoptosis

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138
Q

what are the TNF local effects

A

influx of platelets (clotting helps prevent spread of infection)
efflux of fluid from capillaries (increased flow to lymphnodes, stimulation of adaptive immunity)

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139
Q

TNF can cause pyrexia. what is this and why is it beneficiary

A

fever
inhibits growth of some bacteria/virus
39.5 degrees is the optimum temp for T/B cell activation

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140
Q

when does sepsis occur

A

when conc of TNF is greater than 1microgram/ml

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141
Q

what does sepsis cause

A 
increase vascular permeability leading to hypotension (low blood pressure)
blood clots (heart attacks/ organ damage)
consumpion of clotting factors can lead to internal bleeding/spread of infection
142
Q

what cells can produce interferons

A

all cells of the body

143
Q

what are 2 examples of type 1 interferons

A

IFNα, IFNβ

144
Q

what are type 1 interferons induced by

A

receptors such as RIG-I which detects viral RNA

145
Q

what do type II interferons have a more general role in stimulation

A

immune response

146
Q

what are the responses created by an interferon

A

increased killing of infected cells by increased expression of MHCI so they can be recognised by cytotoxic T cells more easily
activation of NK cells

147
Q

NK cells are programmed to kill unless they get a signal to say that the cell is self. what does this signal come from

A

MHCI proteins

148
Q

interferon γ is which type of interferon

A

type II

149
Q

what does interferon γ have a primary role in

A

adaptive imunity

150
Q

what does interferon γ cause activation of in Th1 response

A

macrophages

151
Q

T helper cells can be further divided into 2 subsets depending on what

A

the cytokines they make

152
Q

what do TH1 cells produce

A

IL-2, IFNγ and TNFα)

153
Q

what do TH1 cells activate

A

macrophages and induce B cells to make opsonising antibodies such as IgG

154
Q

what do TH2 cells produce

A

IL-4, -5, -6, -10, -13

155
Q

what do TH2 cells induce B cells to make

A

IgE

156
Q

what type of response are TH1 involved in

A

inflammatory

classic bacterial and virus infection

157
Q

TH2 cells are important in what type of infections

A

parasitic

158
Q

Different antigens/pathogens induce cells of innate immune system to produce different cytokines. These then act on the adaptive immune system to produce an appropriate response. true/false

A

true

159
Q

what are the main phagocyte in blood

A

neutrophils

160
Q

mast cells are restricted to what

A

tissues

161
Q

eosinophils have recepetors for what

A

C3b, IgG and IgA

162
Q

basophils have receptors for what

A

C3a, C5a and IgE

163
Q

what cytokines do basophils make

A

IL-4 and IL-13 induce TH2 cells. important in parasitic infections

164
Q

what do eosinohpils, basophils and mast cells alll have a role in

A

allergy

165
Q

what do the mast cells make

A

IL-4 and IL-13

166
Q

what does the term professional phagocyte mean

A

their main role is phagocytosis

167
Q

what are the functions of neutrophils (5)

A 
phagocytosis
release of antimicrobials (lysozyme)
production of ROI
production of cytokines
entrapment of microbes
168
Q

what are macrophages derived from

A

monocytes

169
Q

what are 5 examples of reactive oxygen intermediates

A
  • Superoxide
  • Hydrogen peroxide
  • Hydroxyl radicals
  • Hypochlorite
  • Hypochlorous acid
170
Q

what are the steps in which a cell makes ROI

A 
NADPH converts o2 into molecules such as superoxide ion
second enzyme (superoxide dismutase) converts superoxide into hydrogen peroxide
peroxide enzymes convert hydrogen peroxide to hypochlorite ions
171
Q

Phagocytes can also use nitric oxide and other reactive nitrogen species true/ false

A

true

172
Q

where are reactive nitrogen species produced

A

in phagolysosome

173
Q

NK cell activity is controlled by opposing what

A

stimulatory and inhibitory receptors

174
Q

what receptor tells NK cell to kill

A

natural cytotoxicity receptors

175
Q

what is a ligand for natural cytotoxicity receptors (stimulate NK cells)

A

rectin family (abnormally expressed on tumour cells)

176
Q

what receptor causes an NK cell to recognise self proteins and not kill

A

killer immunoglobulin like receptors

177
Q

what molecule tells you that a cell is self

A

MHCI as it is expressed by allcells in the body

178
Q

what is the ability of NK receptors to kill enhanced by

A

presence of interferons

179
Q

where does the dendritic cells transport antigen

A

to lympoid tissue

where it presents the digested antigen to T lymphocytes

180
Q

T and B lymphocytes with appropriate receptors undergo ….. selection in response to an antigen

A

CLONAL

181
Q

what do antibodies exist as (2)

A

integral membrane proteins on B lymphocytes (antigen receptors)
soluble proteins secreted by plasma cells (antigen eliminators)

182
Q

antibodies contain 2 sections Fab and Fc what does this reflect

A

their dual role in immune response

183
Q

what is the Fab arm important in

A

antigen recognition

184
Q

Fab is variable in sequence true/false

A

true

185
Q

Fc region is variable in sequence. true/false

A

false. it is constant

186
Q

what is the main class of antibody in serum and tissues

A

IgG

187
Q

what do the 5 classes of antibody differ in

A

amino acid sequence of the heavy chains

188
Q

studies on antibodies by protein sequencing discovered 3 things. these are

A
  1. antibodies contain constant and variable regions
  2. antibodies are comprised of homologous domains
  3. the variable region domains contain 3 hypervariable regions
189
Q

which region varies the most between antibodies and what does it bind

A

variable region. binds antibody

190
Q

what was thought to be unique to antibodies but now forms the basis of one of the biggest gene superfamilies

A

immunoglobulin fold

191
Q

what is the immunoglobulin gene superfamiliy involved in

A

recognition binding and adhesion

192
Q

the variable region domains of immunoglobulins contain 3 hypervariable regions. what can these also be known as and why

A

complementarity determining regions - determine how well an antibody interacts with its antigen

193
Q

what type of interaction occurs between antibody and antigen

A

non covalent

194
Q

what does the

B cell receptor surface membrane immunoglobulin contain so that it can insert in bilayer

A

around 26 hydrophobic amino acids at C terminus

195
Q

what do most B cells express

A

IgM and/or IgM

196
Q

the B cell receptor can recognise and bind antigen but cannot generate what

A

signal

197
Q

in order to signal what must a B cell receptor associate with

A

Igα and Igβ

198
Q

what do Igα and Igβ contain in their cytoplasmic domain meaning they can signal

A

immunoreceptor tyrosine activation motif (ITAM)

199
Q

T lymphocyte receptor are only expressed on what

A

membranes

200
Q

what do T cells recognise

A

cell associated processed antigen

201
Q

T cells recognised processed peptides presented to then on cell surface by which proteins

A

MHC

202
Q

which class of MHC proteins are expressed on all nucleated cells

A

class I

203
Q

which class of MHC proteins present peptides of exogenous proteins to T helper cells

A

class II MHC

204
Q

which type of T cell recognises endogenous peptides bound to MHCI

A

cytotoxic T cell

205
Q

what does the T lymphocyte receptor have a structure similar to

A

Fab arm of an antibody

206
Q

what does a T lumphocyte receptor comsist of

A

2 chains: alpha and beta.

each with a variable region, constant region, transmembrane region and cytoplasmic tail

207
Q

which part of T cell receptore are the most variable and bind foreign peptide

A

CDR 3 region of alpha and beta chains

208
Q

which parts of T lymphocyte receptors are less variable in structure and bind self MHC

A

CDR1 and CDR2 regions

209
Q

can the T cell receptor generate a signal alone?

A

no

210
Q

what must TCR associate with to generate a signal

A

CD3 subunits

211
Q

what do CD3 subunits contain in their cytoplasmic regions

A

ITAMs (immunoreceptor tyrosine activation motif)

212
Q

how does diversity in antibody receptors arise

A

somatic recombination and mutation of a limited number of inherited gene segments which make up V regions

213
Q

what is the DReyer and Bennett hypothesis (1965)

A

immunoglobulins are encoded by a separate C region and multiple V region genes

214
Q

what was the susumu tonnegawa hypothesis (1976)

A

immunoglobulin genes are rearranged during B cell development

215
Q

what are the 3 sets of immunoglobulin genes

A

heavy chains - chromosome 14
kappa chains - chromosome 12
lambda chains - chromosome 22

216
Q

variable regions are encoded by how many exons

A

2 or more

217
Q

the light chain V regions are encoded by 2 sengments of DNA known as what

A

V and J

218
Q

heavy chain V regions are encoded by 3 segments of DNA known as what

A

V, J and D

219
Q

which heavy chain is always expressed first

A

IgM

220
Q

the V, J and D segments are present in multiple copies in the genome. true/false

A

true

221
Q

during B cell differentiation what happens to V, D and J segments

A

any one can combine with any other segment or give rise to a heavy or light chain

222
Q

how does rearrangement of light chain occuring during B cell differentiation lead to permenant changes in DNA of the mature B lymphocyte

A

one V segment will come to lie nect to one particular J segment.
somatic recombination takes place and intervening DNA is excised

223
Q

which chain rearrangement occurs first

A

heavy

224
Q

what are the simple steps to heavy chain rearrangement

A

particular D segment comes to lie next to particular J segment
joining of particular V segment to recombined D-j segment
intervening DNA excised and lost from cell
all extra bits removed by RNA processing

225
Q

CDR1 and CDR2 are encoded by which parts of heavy chain

A

V segment

226
Q

CDR3 is encoded by which part of heavy chain

A

VDJ join

227
Q

what is a recognition signal sequence (RSS)

A

conserved heptamer (7bp) and nonamoer (9bp) seperated by 12 or 23 nucleotides. found next to coding sequence of V, D or J gene segments

228
Q

what ensure correct VDJ joinging

A

12-23bp rule - a gene segment with a 12bp spacer can only join with a gene segment with a 23bp spacer

229
Q

what is V (D) J recombinase

A

a complex of several enzymes required for somatic V-region gene recombination

230
Q

name 3 types of key enzymes included in V(D)J recombinase

A

DNA cleavage repair enzymes
products of RAG-1 andRAG-2
terminal deoxynucleotide transferase
Artemis nuclease, a member of the ubiquitous non-homologous end joining (NHEJ) pathway for DNA repair.

231
Q

mutations in what can result in SCID

A

RAG-1 and RAG-2 genes or DNA dependent protein kinase

232
Q

what does the RAG-1 RAG-2 complex do during recombination

A

aligns the RSSs adjacent to the gene segments to be joined

233
Q

during recombination a coding joint is made. what is lost from the cell

A

signal joint

234
Q

what are the in depth steps to recombination in heavy chain

A
  1. RSS are recognised by RAG-1 Rag-2 complex and brought together. Induces cleavage in one of the strand which gives reactive OH group exposed
  2. OH group attacks other strand to create double stand break and hairpin
  3. As part of repair process get opening of haripins (can occur symmetrically or asymmetrically)
  4. If asymmetric get overhang which must be repaired with addition of bases on other strands or loss
  5. Particularly in heavy strands you can get nucleotides not encoded in DNA randomly added by deoxynucleotide transferase to give rise to N regions
  6. Get blunt ends formed which can be repaired and brought together by DNA ligase
  7. (have your additional bits of DNA added in)
235
Q

what can happen to unpaired overhangs of DNA hairpin

A

filled in by DNA polymerase

excised by exonuclease

236
Q

what is the main cause of the large diversity in antibodies

A

imprecision of recombination events

237
Q

during combination, if TdT adds nucleotides what can these regions be referred to

A

N regions

238
Q

CDR1 and CDR2 are encoded by which parts of heavy chain

A

V segment

239
Q

CDR3 is encoded by which part of heavy chain

A

VDJ join

240
Q

what is a recognition signal sequence (RSS)

A

conserved heptamer (7bp) and nonamoer (9bp) seperated by 12 or 23 nucleotides. found next to coding sequence of V, D or J gene segments

241
Q

what ensure correct VDJ joinging

A

12-23bp rule - a gene segment with a 12bp spacer can only join with a gene segment with a 23bp spacer

242
Q

what is V (D) J recombinase

A

a complex of several enzymes required for somatic V-region gene recombination

243
Q

name 3 types of key enzymes included in V(D)J recombinase

A

DNA cleavage repair enzymes
products of RAG-1 andRAG-2
terminal deoxynucleotide transferase
Artemis nuclease, a member of the ubiquitous non-homologous end joining (NHEJ) pathway for DNA repair.

244
Q

mutations in what can result in SCID

A

RAG-1 and RAG-2 genes or DNA dependent protein kinase

245
Q

what does the RAG-1 RAG-2 complex do during recombination

A

aligns the RSSs adjacent to the gene segments to be joined

246
Q

during recombination a coding joint is made. what is lost from the cell

A

signal joint

247
Q

what are the in depth steps to recombination in heavy chain

A
  1. RSS are recognised by RAG-1 Rag-2 complex and brought together. Induces cleavage in one of the strand which gives reactive OH group exposed
  2. OH group attacks other strand to create double stand break and hairpin
  3. As part of repair process get opening of haripins (can occur symmetrically or asymmetrically)
  4. If asymmetric get overhang which must be repaired with addition of bases on other strands or loss
  5. Particularly in heavy strands you can get nucleotides not encoded in DNA randomly added by deoxynucleotide transferase to give rise to N regions
  6. Get blunt ends formed which can be repaired and brought together by DNA ligase
  7. (have your additional bits of DNA added in)
248
Q

what can happen to unpaired overhangs of DNA hairpin

A

filled in by DNA polymerase

excised by exonuclease

249
Q

what is the main cause of the large diversity in antibodies

A

imprecision of recombination events

250
Q

during combination, if TdT adds nucleotides what can these regions be referred to

A

N regions

251
Q

before a B cell encounters antigen it is referred to a virgin or naive B cell and expresses what as its receptor(s)

A

IgM or IgM and IgD

252
Q

what happens to a naive B cell if it does not come across ntigen

A

it will die

253
Q

what 2 things can happen when a B cell encounters antigen

A

somatic hypermutation and class switching

254
Q

what does somatic hypermutation of Ig genes depend on

A

deamination of C nucleotides to U by activstion induced cytidine deaminase (AID)

255
Q

where do mutations introduced in Ig by somatic hypermutation tend to be

A

clistered in

CDRs

256
Q

somatic hypermutation can add diversity but what is its main function

A

affinity maturation

257
Q

how does class switching in B cells occur

A

same recombined V region associates with different constant region genes

258
Q

when class switching occurs antige specificity is retained but different effector functions are induced, why is this important

A 
gives a flexible response to pathogen
means you can switch to a class more specialised for the infection you have
259
Q

what does somatic hypermutation and class switching require

A

T cell help and AID

260
Q

class switching occurs by recobination between which regions, with intervening DNA being lost

A

switch regions

261
Q

where are switch regions positioned

A

next to all contant regions genes (coding for IgA, IgE, IgD etc)

262
Q

is class switching reversible

A

no as intervening DNA is lost

263
Q

what initiates class switching

A

AID acting at switch regions

264
Q

AID leads to mutational outcomes. how does this lead to somatic hypermutation in V region

A

most mismatches use mismatch repair and base excision to repair which can give rise to single changes in bases which can change amino acids

265
Q

switch regions are attractive to AID enzymes how does the way the cell repair these lesions lead to class switching

A

cell makes single stranded nicks which lead to double standed nicks and can result in the excision of DNA between the cut switch regions

266
Q

why can IgD be coexpressed with IgM

A

IgD doesnt have a switch region next to it. next to IgM constant region gene there is an IgD constant region gene. makes long RNA transcript that can be processed in different ways

267
Q

why can a B cell making IgA not switch back to making IgM

A

lost the IgM constant region gene

268
Q

why is the class switching mechanism different form VDJ joinging

A

doesnt include RSS sequencs and is not mediated by RAG-1 and RAG-2

269
Q

at the C terminus of IgM there are 2 exons. these make it possible for the production of surface and secreted forms of immunoglobulin. how

A

one codes for hydrophillic amino acid residues and the other hydrophilic. depedning which polyadenylation site is used depends on whether IgM has a hyrophilic (secreted) tail or hydrophobic (surface)

270
Q

the extracellular domains of T cell receptors are homologus to variable and constant regions of immunoglobulins. true/false

A

true

271
Q

how do T cell receptor genes look very similar to antibody genes

A

one constant region gene on alpha chain

2 constant regions in beta chain

272
Q

what 2 chains is a T cell receptor made out of

A

alpha and beta

273
Q

what gene segments do alpha chains in T cell receptors contain

A

V and J

274
Q

what gene segments do beta chains in T cell receptors contain

A

multiple V D and J gene segments

275
Q

which enzymes control the process bt which T cells and B cells randomly assemble different gene segments

A

VDJ recombinase which is a diversecollection of enzymes

276
Q

what gives the biggest diversity of T cell receptor genes

A

junctional diversity at VJ join or VDJ join

277
Q

where is the most diversity concentrated on T cell receptor and why is this important

A

CDR3 region as this is the region that binds to foreign peptide

278
Q

what is different about γδ T cells compared to normal (αβ) T cells

A

γδ T cells do not seem to require antigen processing and major-histocompatibility-complex (MHC) presentation of peptide epitopes

279
Q

what does the MHC play a major role in

A

antigen presentation and initiation of T cell responses

280
Q

having which type of MHC can increase the risk of autoimmune diseases

A

HLA-B27

281
Q

on what type of cells does MHC class I occur

A

all nuclated cells and platelets

282
Q

on what type of cells does MHC class 2 occur

A

can be conditionally expressed on all cell types but normally occurs only on professional antigen presenting cells (macrophages, B cells)

283
Q

which CDRs are not mutated by somatic mutation and bind self MHC

A

CDR1 and CDR2

284
Q

bound peptide is an integral part of MHC protein structure. if they dont have peptide bound to them what does this cause

A

they dont fold correctly without peptide and are not transported to the cell surface correctly

285
Q

how are peptides bound to MHCI expressed on a cell surface

A

misfolded proteins are tagged by ubiquitin and broken down in proteosome
peptides transported to ER by ATP hydrolysis driven transporter TAP
peptides loaded onto MHCI in ER
peptide binding is essential for MHCI cell surface expression

286
Q

how are peptides processed and presented by MHC class II

A 
protein taken up by phagocytosis
fuse with lysosomes whose enzymes cleave protein into may peptides
a particular peptide exhibits immunodominance and loads onto MHC class II molecules.
these are trafficked and externalised on cell surface
287
Q

the MHC genes are very polymorphic with multiple alleles. true/false

A

true

288
Q

where are te polymorphic region in MHC alleles located

A

peptide contact region

289
Q

what are the consequences of polymorphism of MHC

A

graft rejection

290
Q

what are the functions of MHC proteins

A 
graft rejection 
antigen presentation to cells 
T cell activation
self/non self recognition
association with autoimmune diseases
choice of mate
291
Q

when T cells differentiate in the thymus what do they undergo

A

thymic selection

292
Q

T cells bearing T cell receptors that weakly recognise self MHC proteins displayed on the thymus epithelial cells are allowed to survive. this is known as….

A

positive selection

293
Q

T cells that recognise self MHC peptides too strongly are killed this is known as

A

negative selection

294
Q

if they recognise MHCI which which T cell do they become

A

cytotoxic CD8 expressing T cells

295
Q

if they recognise MCHII which T cell do they become

A

CD4 positive T celper cells

296
Q

what percentage of T cells survive thymic selection

A

about 5%

297
Q

people who lack the gene “gene autoimmune regulator” are much more prone to autoimmune diseases. what does this gene allow

A

expression in thymus of proteins found in other parts of the body so that T cells learn not to recognise them (AIRE stimulates this)

298
Q

soluble anitbody proteins meadiate which immune reponse

A

humoral immune response

299
Q

how many subclasses does IgG have and what are they called

A
  1. IgG1, IgG2, IgG3, IgG3
300
Q

which is th anitbody that is present at the highest concentration in serum

A

IgG

301
Q

IgG binds Fc recpetors on which types of cells

A

NK cells and phagocytes

302
Q

IgG is the only class of antibodies that can cross the placenta and has the longest half life of all the antibodies T/F

A

true

303
Q

what in particular is IgG important in

A

young babies immune system through passage from mother

304
Q

what structure does IgM normally exist in in serum

A

pentamer

305
Q

which immunglobulin is the first to appear in serum in response to an antigen

A

IgM

306
Q

IgM is the most efficient of all clases of immunoglobulins at activating complement T/F

A

true

307
Q

does IgM have a hinge region

A

no, it has a functional hinge

308
Q

what structure does IgA have

A

can be monomeric or dimeric

309
Q

where is IgA present

A

in secretions and at mucosal surfaces

310
Q

what does the structure of secretory IgA consist of

A

IgA dimer

+ J chain + secretory component

311
Q

what is IgA present in that is particularly important to newbors

A

milk

312
Q

what does IgA serve as the first line of defence against

A

bacterial and viral antigens

313
Q

what is the role of IgD

A

long been a mystery but we think it plays a role in activation of basophils, white blood cells that have antiparasitiyc function

314
Q

what kind of responses is IgE important in

A

parasitic and allergy

315
Q

what does IgE bind wit high affinity to

A

FcR on mast cells and basophils

316
Q

what is the definition of avidity

A

how tightly a whole antibody molecule binds antigen

317
Q

what is the defintion of affinity

A

how tightly a single Fab arm binds antigen

318
Q

which immunoglobulins are important in preenting the binding of pathogens to host cells

A

IgG and IgA

319
Q

which immunoglobulin is important in aglutinaitng particles eg bacteria

A

IgM and IgA

320
Q

which immuglobulins activate complement

A

IgM and IgG

321
Q

which immunoglobulins bind Fc receptors on leukocyte surfaces

A

IgA IgG and IGE

322
Q

what does complement activation result in

A

infammation, activation of leukocytes, opsonisation and lysis of foreign cells

323
Q

why are the functions of complement important

A

helps body get rid of immocomplexes

inducer of inflammation

324
Q

what causes SLE

A

body not being able to clear immunocomplexes efficiently

325
Q

what kind of receptors are expressed by a variety of effector cells

A

FcR (Fc receptors)

326
Q

what do Fc receptors bind to

A

antibodies that are attached to infected cells or invading pathogens.

327
Q

There are several different types of Fc receptors (abbreviated FcR), which are classified based on the type of antibody that they recognize. how do we name Fc receptors for the differemt antibodies

A

ype of antibody is converted into the corresponding Greek letter, which is placed after the ‘Fc’ part of the name. For example, those that bind the most common class of antibody, IgG, are called Fc-gamma receptors (FcγR

328
Q

what do activation FcR contain on their intracellular tail

A

ITAMS (imunoreceptor tyrosine activation motifs)

329
Q

what do inhibitory FcR contain on their intracellular tail

A

ITIMs (immunoreceptor tyrosine inhibitory motifs

330
Q

When IgG molecules, specific for a certain antigen or surface component, bind to the pathogen with their Fab region (fragment antigen binding region), their …………. point outwards, in direct reach of phagocytes.

A

Fc regions

331
Q

interactions between the Fc region of the antibody and the Fc receptors of the phagocyte result in what?

A

the initiation of phagocytosis

332
Q

what is frustrated phagocytosis

A

phagocyte may come across something that is too big to phagocytose. releases the contents from its granules (reactive oxyge intermediates etc)

333
Q

what are the Fc receptors on Nk cells that bind IgG known as

A

FcγRIII (CD16)

334
Q

cross linking of Fc receptors signals NK cells to kill the target cell. what is the method of killing

A

ADCC (antibody dependent cell mediated cytotoxicity)

335
Q

FcγRIII on NK cells can also associate with monomeric IgG (i.e., IgG that is not antigen-bound). When this occurs what happens

A

the Fc receptor inhibits the activity of the NK cell

336
Q

TRIM21 is an intracellular Fc receptor for which immunoglobulins

A

IgG, IgA and IgM

337
Q

is TRIM21 part of the immunoglobulin super gene familty

A

no

338
Q

what does TRIM21 (fc receptor) mediate

A

intracellular humoral immunity (allows anitbody to directly kill

339
Q

what does TRIM21 fc receptor do

A

• Recruits to internalised antibody bound virus, adds ubiquitin label and targets virus to proteasome

340
Q

what is FcRn

A

neonatal Fc receptor for IgG

341
Q

is FcRn a memebrr of the immunoglobulin superfamily

A

no

342
Q

FcRn receptors can also be present in aldults. what do these doe

A

stops IgG from being lost from the body. takes up IgG and stops it from being degraded

343
Q

what do Fc receptors on mast cells and basophils medaite

A

allergy/defense agains large parasites (bind IgE)

344
Q

what does cross linking of Fc receptors on mast cells cause

A

them to release their granular content

345
Q

what influences the class of antibodies made in the humoral response

A

type of cytokines that T cells make

346
Q

production of effector T cell from a primed or memory or effector cell requires how many signals

A

1

347
Q

production of effector T cell from naive T cell requires how many signals

A

2

348
Q

what 1 signal do primed or memory or effector T cells need

A

recognition of MHC and peptide and coreceptro

349
Q

what 2 signals do Naive T cells need to be activated

A
  1. recognition of MHC + peptide + coreceptor (CD4/CD8)

2. recognition of co strimulatory signal

350
Q

where are costimulatory molecules expressed for the production of effector T cells

A

dendritic cells, macrophages and B cells

351
Q

give an example of a costimulatory signal

A

B7 which is expressed by dendritic cells, macrophages and B cells

352
Q

what does the costimulatory molecule B7 bind to and what does this induce the expression of

A

CD28 inducing the expression of IL-2 and IL-2 receptor. this acts in autocrine fashion on T helper cells and is also required for cytotoxic T cell activation

immunology (3 decks)

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