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1
Q

what is the immune system?

A

A system of cells and molecules designed to fight infection

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2
Q

Name some infectious agents

A 
Worms: tapeworm
Protozoa: malaria
Funghi: Aspergilus Candida
Bacteria: Staphylococcus
Virus: Influenza
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3
Q

What are the three layers of defence

A

Physical Barrier- Skin
Innate immune system- primary response
Adaptive Immune system-immunological memory

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4
Q

how is the skin protective

A

Impermeable barrier
when damaged- infection more of a problem
prevents bacteria living on skin- done through inhibitory lactic acid and fatty acids in sweat and subaceous secretions
low pH
(sebum secreted from subaceous glands makes skin waterproof and waxy)

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5
Q

What is the difference between the innate and adaptive immune system

A

innate system is broadly specific- recognises similar structures in pathogens but reponds the same way everytime it sees the same pathogen
Adaptive immune system- highly antigen specific. Immunological memory much stronger and faster response the second time it meets an antigen
in reality not discrete systems- form a continuum

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6
Q

what anti microbal functions do secreted fluids contain?

A 
Gastric secretion: acid
Semen: Spermine and zinc
Milk: Lactoseperoxidase
Tears, nasal secretion, saliva: Lysozyme
(not part of the immune system)
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7
Q

how does mucous protect against infection

A

secreted by lining of inner surface of body
prevents the adhesion of microbes to epithelium preventing colonisation
traps microbes

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8
Q

How do physiological bacterial flora protect against infection?

A

they compete with invading microbes for nutrients for growth
produce microbicidal substances
antibiotics that kill bacterial flora make infection more likely

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9
Q

What is an antigen

A

an organism or molecule recognised by the immune system

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10
Q

what are the cells of the innate immune system?

A 
Phagocytes: monocytes macrophages and neutrophils
Eosiniphils
Mast cells + Basophils
Dendritic cells
Natural Killer cells
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11
Q

what are phagocytes provide 3 examples and where they are derived from?

A

phagocytes use pseudopodium to secure target and engulf them and digest using chemicals

  • monocytes (mononuclear phagocytes) found in blood short lived
  • macrophages derived from monocytes, leave blood and enter tissue- longer life span
  • neutrophils (granules in cytoplasm, lots of cytoplasm, single multilobed nucleus)- fairly short lived produced continuously, found in blood and tissue at site of infection
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12
Q

what do eosinophils do?

A

two or three lobed nucleus, lots of cytoplasm
can phagocytose small molecules
release toxic molecules onto surface of organisms too large to phagocytose e.g parasitic worms
(stain with eosin [H and E stain])
secrete major basic proteins, cationic proteins, oxygen metabollites ( e.g. superoxides) and perofins

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13
Q

whats the difference between mast cells and basophils

what do they do

A

mast cells found in tissues, basophils found in blood, derived differently

result in inflammation

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14
Q

what are dendritic cells

A

-one of the main links between innate and adaptive immune systems
involved in activating immune system- present antigens to t cells through MHC class II
-in skin as immature langerhans cells and lymphoid organs
internalise
-express CD80 and CD86
(CD86 binds to CD 28 on t cells)
activate B cells
required for T cell activation

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15
Q

what are NK cells

A

-have a round nucleus with small amount of cytoplasm.
-kill extracellularly
exactly
-kill all cells that don’t express MHC I

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16
Q

what molecules are used by the innate immune system

A

Complement
acute phase proteins e.g CRP
interferons- IFN-α IFN-β, IFN-γ - interfere with viral replication

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17
Q

what are the cells of the adaptive immune response?

A

T lymphocytes- Th, Tc, Treg
B lymphocytes
antibodies

look similar to NK cells

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18
Q

What does Th do

A

helper T cells

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19
Q

What does Tc do

A

kills infected cells

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20
Q

What does Treg do

A

supress immune system response

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21
Q

what do antibodies (Ab) do

A

directly neutralise toxins and viruses
link different parts of immune system
recruit phagocytes, killer cells or complement

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22
Q

when is the immune response activated

A

within 0-4 hours of threat- recognition by nonspecific and broadly specific effectors

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23
Q

macrophages

A

derived from monocytes- from bone marrow
active in tissues especially spleen and lymph
phagocytes
pathogen recognition receptors induce other receptors- induce oother reactions, produced cytokines

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24
Q

what are the two types of Dendritic cells

A

follicular dendritic cells

dendritic cells

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25
Q

what is the difference between dendritic cells and follicular dendritic cells

A

dendritic cells are wide spread,
express: MHC class II, CD80,86
process antigen to T cells
phagocytosis

follicular dendritic cells in germinal centre
dont have MHC class II or CD80,86
do not phagocytose
native antigen to B-cells

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26
Q

Follicular dendritic cells

A

only in secondary lymphoid tissue- spleen and lymph nodes
activate B cells
no MHC II or CD80/86
cant phagocytose

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27
Q

how do FDC activate B cells

A

present native antigen to B Cell
B cell recognises antigen antibody complex
brought to centre of germinal lymphoid tissue
activates B cell which matures
IgG response- highly specific antibodies

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28
Q

what % of NK cells circulate

A

2%

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29
Q

what is missing self

A 
'missing self' is what NK cells recognise
they kill cells that do not express MHC class I which all of our cells possess therefore they kill if no protein or antibody is recognised- missing self
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30
Q

give an example of an infection that avoids death missing self

A

cytomegalovirus
modifies MHC class I so it is still recognised
however it can still be killed by NK cells through many activator molecule being expressed that inhibit the recognition of MHC I causing NK cells to be activated anyway

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31
Q

what are Pattern recognition receptors?

A

found on neutrophils, macrophages, DC

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32
Q

where are the acute phase proteins produced

A

liver
IL 1 IL 6 TNF activate

causes release of C3 (part of complement)
CRP (activates complement)
fibrinogen- cogagulation

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33
Q

What are the three ways to activate complement?

A

Classical pathways
Lectin
Alternative

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34
Q

What cleaves c5 and c3

A

C3: c4b2a, c3bBb

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35
Q

What is the membrane attack complex

A

C3a, c3b, c5a, c6, c7, c8, c9

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36
Q

Explain opsinisation

A 
TLR recognises microbe
Complement C3b added to microbe
Antibody added in same way
Phagocyte has C3bR and antibody R 
Antibody+ complement activates phagocyte
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37
Q

what is inflammation

A 
tissues response to injury or infection
characterised by the increased blood flow and entry of leukocytes into the tissue
results in:
swelling
redness
elevated temp
pain
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38
Q

what is complement

A

a set of around 20 proteins that act in an enzymatic amplification cascade to activate components involved in immune response

  • perform opsinisation
  • cell lysis (membrane attack complex)
  • enhance inflammation

travels around blood is inactive soluble proteins

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39
Q

what proteins are in the classical pathway?

A

C1q C1r C1s-> C4b2a- c3 convertase

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40
Q

what makes up the MAC

A

C5b C6 C7 C8 C9 (many C9s)

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41
Q

where do T cells develope

A

Thymus in chest cavity ( from bone marrow)

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42
Q

when do T cells express both CD4 and CD8

A

when immature

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43
Q

what T cells are CD4+

A

T helper

Treg

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44
Q

what cells are CD8+

A

Tc

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45
Q

what are the two forms of TCR

A

alpha beta

gamma delta- rare

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46
Q

what are the regions of the TCR

A

V- variable- recognises peptide MHC complex

C-constant

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47
Q

what is the structure of the TCR

A 
2 chains ( usually alpha and beta) linked by disulphide bonds
each chain has a variable region, a constant region and a transmembrane region
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48
Q

what does the the alpha beta TCR recognise?

A

the antigen presented by MHC on an antigen presenting cell

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49
Q

what class of MHC does CD8 bind to

A

CD8 (cytotoxic Tcells) bind to MHC class 1

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50
Q

what class of MHC does CD4 bind to?

A

CD4 (cytotoxic T cells) binds to MHC class 2

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51
Q

what is the co receptor of TCR

A

CD3 co receptor
made up of 1 gamma, 1 delta, 2 epsilon,
2 zeta

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52
Q

how does LCK work

A

LCK recognises ITAM region of CD3 and zeta chains and phosphorylates a tyrosine group to activate if a pathogen is presented to TCR

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53
Q

what is the TCR complex

A

TCR CD3 + 2 zeta chains

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54
Q

how many different types of TCR is on a single T cell

A

1

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55
Q

what are the 2 forms of selection of T cells

A

positive selection- recognise own MHC

negative selection- recognises self antigens

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56
Q

what is anergy

A

an unactivated T cell

TCR + MHC II + CD4 not enough

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57
Q

describe the process of T cell activation

A

xx

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58
Q

how many B7 molecules exist on antigen presenting cells

A

B7.1-CD80

B7.2-CD86

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59
Q

what are the functional activities of T cells

A

Proliferate (specific for pathogens)
mediate effector response
form memory cells

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60
Q

what is the function and what are expressed/produced by Th1

A 
help Tc and macrophages
inhibit Th2
IFN gamma
IL-2
TNFbeta
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61
Q

what is the function and what are expressed/produced by Th2

A 
help B cells produce antigens
inhibit Th1
IL-4
IL-5
IL-10
IL-13
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62
Q

what is the function and what are expressed/produced by Th17

A

pro inflammation
IL-17
IL-22- more important

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63
Q

what is the function and what are expressed/produced by Tfh

A

help germinal centre B cells
IL-21
ICOS

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64
Q

what is the function and what are expressed/produced by

Treg

A

suppress immune system
TGFb
IL-10
IL-35

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65
Q

what is the function and what are expressed/produced by

Tc (CD8+)

A

Perforin
Granzymes
FasL
Cytokines

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66
Q

how does Th1 activate macrophages

A

TCR-MHC
CD40L->CD40R on macrophage
IFN gamma released- super activates

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67
Q

how does Th1 activate Tc

A

-releases IL2 and IL6 to enhance Tc cells- co stimulation

+MHC I and TCR

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68
Q

methods of cytotoxic T cell killing

A

Granule dependent killing- perforin makes holes
fasL binds to target
caspase activation apoptosis

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69
Q

what distinguishes a T cell from a B cell

A

look the same microscopically
T cells express CD4 or CD8
B cells express antigens

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70
Q

What are the five classes of antibodies?

A 
IgG
IgA
IgM
IgD
IgE
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71
Q

where are B cells produced

A

Bone Marrow

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72
Q

what do naive B cells express?

A 
IgM and IgD
Ig alpha Ig Beta- not actual antibodies
CD19-marker for B cells
CD20-marker for B cells
CD40
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73
Q

what is an antibody made up of?

A

variable region and constant region

recombination of variable region makes 10^15 different antibodies.

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74
Q

what does the variable region do?

A

recognises antigen

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75
Q

what is clonal selection

A 
presence of antigen specific for an antigen leads to the reproduction of the antigen
Ig alpha and Ig Beta stimulated
2 types of cells produced:
Plasma cells- secrete antibodies-
Memory cells- express antibodies on surface
(T cells 
2 types of cells: 
effector cells 
memory cells
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76
Q

how many different constant regions are there ( of antibodies)

A

3

Cµ Ckappa Clambda

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77
Q

adaptive immune response

A

qualitatively and quantitatively better

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78
Q

how does class switching of antigens happen

A 
requires MHC presenting antigen from B cell to Th2 (best at class switch)
Th2->B cell
CD28->B7
D40L->CD40R
cell contact dependent
\+cytokines
mutual activation
B cell enters cell cycle
Cytokines direct class switching
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79
Q

what cytokines direct IgE switch

A

IL4 and IL12

inhibited by gamma interferon

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80
Q

what is somatic hyper mutation

A

in variable region of antibody, proof reading down regulated
each replication chance of mutation- increases variability but can lead to defunct antibodies- stop codon
can be massively favourable

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81
Q

how do FDCs enhance immunomemory

A

store small amount of antigen for a long time- stops memory cells from dying

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82
Q

what MHC class do B cells have

A

MHC class 2

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83
Q

which cells have MHC class II

A

professional antigen presenting cells

B cells, DC, macrophage,

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84
Q

explain the action of B cells in presenting an antigen to a t cell

A

Antibody binds antigen
antibody +Ig alpha+ Ig beta (=whole receptor) src family tyrosine kinases phosphorylates tyrosine in ITAM on Ig alp and beta
antigen brought into B cell by endocytosis of antigen antibody complex
antigen degraded
intake of antigen activates B cell
presented in MHC classII

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85
Q

T cell independent

A 
polysacharide- shape of molecules brings antibodies close together in membrane doesnt require T cell activation
no t cell no class switching
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86
Q

T cell dependent

A

need T cell interactions CD40 L, CD28

cytokines

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87
Q

what are the 4 types of receptors in the immune system

A 
pattern recognition receptors e.g TLR
MHC class 1: HLA A, HLA B, HLA c
class 2: DP, DQ, DR
TCR
BCR
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88
Q

what is the structure of an antibody?

A

2 heavy chains

2 light chains

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89
Q

what is the complementarity determining region

A

a part of the antibody that is highly variable and is complementary to an antigen

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90
Q

where does the variability of antibodies come from?

A

recombination of the CDR

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91
Q

where is the heavy gene located

A

Chr 14

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92
Q

what are the 2 forms of light chain

A

Kappa Chr 2

lambda Chr 22

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93
Q

what are the gene segments that make up the heavy chain involved in recombination

A

Variable (V)- 40 genes
Diversity (D) -27 genes
Joining (J)- 6 genes
constant (C)- 9 genes

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94
Q

describe the process of recombination

A

(randomly) one D put next to a J

V recombines with DJ splice out introns get a VDJ sequence

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95
Q

how many heavy chains do you have

A

2 copies one from each parent

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96
Q

how many light chains

A

2 kappa 2 lambda

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97
Q

which enzyme is responsible for V-D-J recombination

A

recombinase enzymes encoded by RAG1 RAG2

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98
Q

what do RAG1 and RAG2

A

recognises recombination signal sequence (RSS)

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99
Q

what is the 12 23 rule

A

you can only recombine a gene with 12 space RSS wit hone with 23 space RSS
D- 23
J-12
V-12
can only combine v with D and J with D not J with V or D with D

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100
Q

how do you get additional diversity in antibodies

A

recombinatorial inaccuracies- recombine DNA location of splice
N-nucleotide addition- Terminal deoxynucleotidyl transferase TdT
Chain combinations
Somatic hypermutation- each division of cell is a chance for mutation

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101
Q

what does class switching of antibodies involve

A 
changing constant recion of heavy chain
IgG- Gamma
IgA- alpha
IgM-mu
IgD-delta
IgE-epsilon
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102
Q

what are the 4 subclasses of IgG

A

IgG 1
IgG2
IgG3
IgG4

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103
Q

what are the 2 light chains of an antibody

A

Kappa and lambda

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104
Q

what connects the two heavy chains of the antibody

A

hinge region with disulphide bonds

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4
5
Perfectly
105
Q

give two examples of antibody monomers

A

IgM- pentamer in circulation

IgA dimer in mucosal surface

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106
Q

where can antibodies be found

A

cell surface

soluble

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107
Q

what is an epitope

A

region of antigen that an antibody can bind to
always a similar size no matter how big an antigen is
a bigger antigen will just have more epitopes

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108
Q

what is a discontinuous epitope

A

amino acids from all over the antigen fold to be close to each other

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109
Q

what is a continuous epitope

A

when aas are next to each other in a sequence (primary sequence)

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110
Q

what forces are involved in binding antigen and antibody

A

H bond
electrostatic forces
hydrophobic interaction
van der waals

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111
Q

what is a single arm of an antibody

A

Fab

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112
Q

why do antibodies have 2 arms

A

more chance to bind to an antigen

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113
Q

by how much does the IgM pentamer increase the chance of binding to antigen

A

10^7 increase in equilibrium constant

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114
Q

how can more than 1 antibody bind to a single antigen

A

different epitopes on a single antigen

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115
Q

what is the most common antibody

A

IgG

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116
Q

how does an antibody stay in a membrane

A

many hydrophobic aas far down stream from CDR

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117
Q

how are antibodies secreted

A

hydrophobic aas removed

118
Q

which antibodies work best alone

A

IgM and IgG

119
Q

antibodies acting on their own

A

bacterial toxin- stopped from entering cell by Ab binding
block viruses- binds to receptors on viruses
bacteria- blocked from binding to mucosal surface

120
Q

how do antibodies link to other parts of immune system give 3 examples

A

RBC -complement receptor (Cr1)- recognise antibody antigen complex
C3b taken to liver and spleen
-FC gamma- receptor on phagocytic cells respond to IgG
IgG opsinises cells for phagocytosis
-IgM and IgG activates MAC
-antibody dependent cell mediated cytotoxicity
FC gamma R on NK cells- release toxic molecules
-IgE causes mast cells to degranulate. FC epsilon R

121
Q

what is the function of IgM

A

antigen receptor on naive B cells (monomer)
when released from plasma cell- pentamer
first antibody produced in immune response
activate compliment

122
Q

what is the function of IgG1

A

activates compliment
enhances phagocytosis
can cross the placenta
(in breast milk)

123
Q

what is the function of IgG2

A

activate compliment

124
Q

what is the function of IgG3

A

activate compliment
enhance phagocytosis
can cross placenta

125
Q

what is the function of IgG4

A

can cross placenta

126
Q

what is the function of IgA(1 and 2)

A

protect mucosal surface

127
Q

what is the function of IgD

A

antibody on naive B cell

128
Q

what is the function of IgE

A

release of inflammatory mediators from mast cells

allergy

129
Q

where are HLA genes expressed

A 
HLA genes are the genes of MHC class 1
they are expressed on all nucleated cells
130
Q

where are MHC class 2 expressed

A

professional antigen presenting cells
dendritic cells, B cells, macrophage
(professional antigen presenting cells will express both MHC class 1 and class 2)

131
Q

what is MHC class 3

A

involved in immune response eg complement

132
Q

what is the function of MHC class 1

A

alert cytotoxic T cells to intracellular infection

133
Q

what is the function of MHC class 2

A

specialized for activating helper T cells

134
Q

which HLA (MHC class 1) gene is most polymorphic

A

HLA-B

HLA-C is least variable

135
Q

where is there high variation in the population MHC genes

A

pathogens are constantly changing we need a wide range in the population so the entire population isnt wiped out

136
Q

what is the structure of MHC molecules

A

2 sausages on a BBQ
5 Beta sheets
2 alpha helices- form the groove in which the peptide sits

137
Q

which chain is more variable in MHC class 1

A

Alpha

only 1 Beta variety

138
Q

what is the domain structure of MHC class 1

A 
00
o0
/
0=alpha 1/2/3
o=beta 2 microglobulin
/=transmembrane
groove between alpha 1 alpha 2
139
Q

what happens if ß2 microglobulin is KOed

A

the MHC molecule will not reach the cell surface

140
Q

what is the domain structure of MHC class 2

A 
0o
0o
/ /
0=alpha 1/2
o=beta 2 microglobulin
/=transmembrane
groove between alpha and beta
141
Q

what is the difference between MHC I and MHC II

A

MHC II can bind larger pieces of antigen as it is not closed at the ends of the groove. open grooves allows larger peices to bind

142
Q

do all regions of the MHC binding groove contribute equally

A

no anchor positions more important
position 5 Y/F
position 8 L/M/I/V
sequence of aas only important at anchor regions

143
Q

co stimulation of MHC I to TCR

A

Tc- CD8 recognises non polymorphic part of MHC

CDR of TCR bind to protein and polymorphic region of MHC

144
Q

what happens to the cell when an infection happens

A

immunoproteasome formed
switch on of genes associated to the proteasome
immunoproteasome chops up to the correct region for MHC I

145
Q

how big is the region of antigen presented on MHC I and II

A

endogenous proteins- MHC I- 8-9 aas long

exogenous MHC II- 15 aas long

146
Q

how does an antigen get presented onto MHC class 1

A

syntesis of MHC in RER
calnexin binds to alpha chain to make it bind to ß2 microglobulin
calreticulin 57 keeps MHC in correct shape for antigen to bind
Transporters associated with antigen processing (TAP) 1 and 2 pick up protein cleaved by immunoproteasome and takes it to RER (active)
put into MHC
MHC taken to cell surface

147
Q

how does a protein get presented to MHC class 2

A

antigen phagocytosed binds to proteasome broken down to the correct shape
invariant chain produced by RER and put into MHC groove prevents anything else binding
MHC II moves to endosome containing the correct length protein
most of invariant chain degraded, some remains called CLIP
DO and DM remove CLIP from groove
MHC taken to membrane

148
Q

what is cross presentation

A

the ability of MHC class 2 to present endogenous peptides and MHC class 1 to present exogenous

149
Q

can an MHC reach the cell surface without a peptide

A

no

150
Q

which motile system do immune cells use

A

Blood

Lymph

151
Q

what lets immune cells into the lymph node

A

HEV

high endothelial venules

152
Q

how do lymphocytes/ immune cells reach the inflammed tissue

A

histamine increases the gaps in the endothelium of blood vessels allows immune cells into the inflammed tissue
histamine acts as chemotactic gradient

153
Q

when does an immune cell stay in the lymph node

A

if an antigen is present a cell will stay in the lymph node otherwise it leaves

154
Q

what is the structure of the lymph node

A

cortex- mostly B cells
paracortex mostly T cells
medulla

155
Q

what brings antigen to lymph node

A

Dendritic cell recognises antigen with PRR (TLR)
moves out of tissue into lymph node
(no longer phagocytic)
upregulates CD80 CD86

156
Q

what happens when an antigen is in a secondary lymphoid tissue

A

follicle produced

becomes secondary follicle with germinal centre in the middle

157
Q

what are the structures of germinal centres

A 
Mantel zone round the edge- less densely packed
dark zone
basal licht zone 
apical light zone
naive B cells move from top to bottom
158
Q

what do FDC do

A

present antigen to naive B cell

have immune complexes of antigen, antibody and complement

159
Q

what cells are in the germinal centre

A 
B cells
T cells (Tfh)
DC
FDC
macrophage
160
Q

what happens in germinal centre

A

B cell class switching
affinity maturation
memory cell generation
plasma precursor generation- plasma cells would cover antigens on FDC

161
Q

what are the similar structures to germinal centre in spleen?

A

periarteriolar lymphoid sheath
Red pulp
white pulp-b cells
germinal centre in the middle

162
Q

how does the mucosal surface protect against infection

A

IgA in mucous
dimer joined by joining chain and secretory component derived from poly Ig receptor- binds to polymerised antibodies
secretory part
cleaves receptor bound to secretory part
plasma cells producing IgA underneath mucosa

163
Q

what is the role of IgE

A

back stop
Mast cells express FC epsilon receptor which is very high affinity for IgE so essentially is coated with IgE
when it binds to an antigen causes degranulation- release of histamine and chemotactic factors that draw neutrophils and eosiniphils into the tissue

164
Q

peyer’s patch of gut

A

m (microfolded) cells at base of villi in lamina propria
antigen transported to it generation of thymine follicle and then secondary follicles with germinal centre
lymphocytes activated leave peyer’s patch go to mesenteric lymph nodes where they are fully activated and go back to gut

165
Q

how do lymphocytes home to intestine

A

mucosal Addressin cell adhesion molecule 1 (MAdCAM1)on blood vessel in endothelium interacts with integrin alpha4 Beta7 on lymphocyte
MAdCAM1 only in gut endothelium brings them back to gut

166
Q

what are the 2 types of communication in immune response

A

cell-cell contact dependent

soluble molecule

167
Q

what size are thesecreted molecules

A

8-80kD

168
Q

what are the functions of diffusable signallling

A

hematopoesis control

immune response

169
Q

groups of cytokines

A 
Interleukins
colony stimulating factors
chemokines
interferons
tumour necrosis factor
GF
170
Q

give an example of pleiotropy in cytokines

A

IL4
B cell activation and proliferation
Thymocyte and mast cell proliferation

171
Q

give an example of redundency in cytokines

A

IL 2, IL5, IL4 all cause B cell proliferation

172
Q

give an example of synergy in cytokines

A 
IL4 can cause class switching of antibodies
IL4+IL5- much more efficient
173
Q

give an example of antagonism in cytokines

A 
IL4 causes class switching
IL4+INF gamma- inhibits class switching
174
Q

give an example of a cascade involving cytokines

A

IFN gamma produced by Th cells

activates macrophages which produce IL12 which stimulates Th cells

175
Q

which cytokines are proinflammation

A

IL-1 IL-17

176
Q

which cytokines are immunosuppressive

A

IL-10, TGF ß

177
Q

which cytokines are antiviral

A

IFN alpha, IFN gamma

178
Q

which cytokines are T cell proliferation

A

IL-2, IL-12

179
Q

B cell proliferation

A

IL-2, IL-13

180
Q

Haematopoiesis

A

M-CSF, GM-CSF

181
Q

Chemotaxis

A

IL-8 (CXCL8), RANTES (CCL5)

182
Q

therepeutic use of cytokine

A

IFN alpha for viral infections
rheumatoid arthritis- anti TNF alpha- blocks
genetically engineer soluble TNF receptor works the same as an antibody in RA

183
Q

what is auto immune disease

A

when auto antibodies are produced and T cells that act on our own cells becoming pathological

184
Q

what is central tolerance

A

specificity to our own cells in T and B cells in Thymus and Bone marrow

185
Q

explain positive and negative selection in thymus

A

T cell is double negative
T cell becomes double positive
Positive selection- TCR can recognise our own MHC. binding to MHC I and II in thymic epithelium prevents death of T cell by stoping apoptosis. the default pathway is to die
Negative selection- apoptosis enduced in cells that have high affinity for self MHC + self protein

high affinity for MHC I- CD4 turned off
High affinity for MHCII CD8 turned of
become single +ve T cell

186
Q

what removes dead T cells in thymus

A

Macrophages

187
Q

how do self antigen reach thymus

A

hormones in blood

188
Q

how do tissue specific proteins get to thymus?

A

AIRE (autoimmune regulator) TF causes the thymic expression of tissue specific genes

189
Q

what is peripheral tolerance

A

the removal of self reactive lymphocytes that escape central tolerance

190
Q

how B cells undergo central tolerance

A

clonal deletion

receptor editing- removal of self antibody for an active one

191
Q

what are the two mechanisms of peripheral tolerance

A

Clonal anergy

suppression

192
Q

describe anergy

A

the induced inactivation of a T/b cell
if the only stimulation is CD4 + TCR MHC II cell inactivates
reactivated by IL2

193
Q

how can you increase costimulatory factors?

A

PRR recognises PAMPs increases transcription of CD80, CD86 to activate CD28 on T cell and cause activation
if self antigen- no PAMPs no stimulation

194
Q

how do Treg cells

A

express FOXP3 and CD25
(foxp3 can be stimulated through an antigen)
secrete IL10 and TGF ß (immunosuppressive)
release cytotoxic granules
mop up IL2- reduced lymphocyte proliferation and differentiation
removes CD80/86 from antigen presenting cells by using CTLA4

195
Q

what is autoimmune disease

A

the result of a breakdown of immunological tolerance

196
Q

give 3 examples of tissue specific autoimmune diseases

A

MS
Hashimoto’s disease
Type I diabetes

197
Q

give two examples of non tissue specific autoimmune disease

A

SLE- antinuclear antibody
dermatomylitis
RA-IgG antibody against IgGFc

198
Q

what causes autoimmune disease

A

Genes- e.g. MHC, CTLA-4
if 1 identical twin gets an AI disease increases chance of other one to 50%
more common in female than males

environment-stress, infection

199
Q

give 2 examples of MHC genes leading to AI disease

A

Ankylosing Spondylitis- HLA B27 increases chance of getting disease by 87%
antigen mimickry
Rheumatic fever
streptococcus group A antigen that looks likecadiac myosin

200
Q

WHAT IS HASHIMOTOS THYROIDITIS

A

anti body against thyroid peroxidase
inflammation of thyroid
Tc cells kill thyroid
enlarged thyroid

201
Q

SLE

A

antinuclear antibodies

immune complex trapped in capillaries and glomeruli

202
Q

Graves disease

A

TSH R overstimulated

203
Q

what is allergy

A

immune response to what should be harmless

204
Q

What are the 4 types of hypersensitivity

A

Type 1
type 2
type 3
type 4

205
Q

what is type 1 sensitivity

A

IgE mediated mast cell degranulation
e.g asthma
IgEs bind to different epitopes of antigen
allergen causes cross linking of Fc epsilon R starts signalling cascade
degranulation of mast cells- histamine + serotonin released
synthesis of TNF alpha and prostaglandins and leukatryins
late phase response (5-12hours) mediated by CD4+ helper T cells

no allergy gene

206
Q

what is type 2 sensitivity

A

cytotoxic antibody against cell surface antigen
e.g transfusion reaction/ transplant rejection
IgG antibody dependent
Killer cells with Fc receptor +IgG recognises antigen on target causes release of cytotoxic products

Complement mediated cell lysis

macrophage engulf target

207
Q

what is type 3 sensitivity

A

Immune complex mediated
e.g SLE
antibdoy antigen complex not cleared aggregates attracts complement
C3a and C5a increase inflammation +platelet aggregation+ IL1 and TNF
chemotaxis of neutrophils C5a- tissue damage

208
Q

what is type 4 sensitivity

A

Delayed type hypersensitivity
T cell mediated
e.g tuberculin skin reaction mycobacterial antigens
contact dermititis to nickel
eosiniphils cause damage to tissue
macrophages enlarge- form multinucleated macrophages- can cause granuloma- seal off area
Tc cells kill target

209
Q

how do you test for allergy

A

patch test on skin

patch of pure antigen put on skin

210
Q

treatment of type 1 hypersensitivity

A

avoid allergen

corticosteriods- block TF of proinflammatory genes
sodium chromoglycate- blocks mediator release from mast caells
antihistamine
montelukast

immunotherapy sublingual immuno treatment (SLIT)
small amount of allergen (not enough to produce response)
anti IgE- reduces IgE and therefore Fc epsilon R

211
Q

hygeine hypothesis

A 
clean environment increases Th2 to Th1 causes class switching to IgE
soap removes protective secretions by skin
212
Q

Haemolytic disease of the fetus

A

Type 2 hypersensitivity
rhesus incompatibility

example
mother RhD- father RhD+
child Rhd+

birth only time fetal RBC enters mother. mother makes anti RhD+ antibodies
no problem in first pregnancy
second pregnancy secondary response-> haemolytic disease of the fetus

treatment
after birth mother given IgG anti D- mops up fetal RBC doesnt sensitise mothers B cells

213
Q

innate hypersensitivitytoxic shock caused by stapylococcus aureus

A

excess release of TNF and IL1 and IL6

acute respiratory distress syndrome

214
Q

what is an autograft

A

graft from same individual

one part of body to another e.g skin graft

215
Q

what is an iso graft

A

graft between identical individuals

e.g twins

216
Q

what is an allograft

A

between different members of same speicies

217
Q

xenograft

A

from different species

e.g pig heart

218
Q

explain the a strain and B strain mouse thing

A

A graft onto A mouse=accepted
B graft onto A mouse=rejected
B graft onto AB mouse= accepted
AB graft onto B mouse rejected

219
Q

T cell transfer

A

A mouse + B graft–>t cells–> A mouse + B graft- secondary response

A mouse + B graft–>t cells–> A mouse + C graft- primary response

A mouse + C graft–>t cells–> A mouse + B graft- primary reaction

220
Q

recognition of graft antigen: 2 pathways

A

Direct

Indirect

221
Q

explain the direct pathway

A

allo MHC different to host MHC
TCR recognises foreign MHC and peptides
T cell attacks

222
Q

Indirect

A

donor cell- MHC removed when entering recipient

broken down and presented as antigen to host

223
Q

what is graft versus host reaction

A

e.g bone marrow transplant, host immunosuppressed- graft attacks host

224
Q

what tissue does not need to be typed before transplant

A

cornea- no blood supply

pig heart valves

225
Q

all grafts eventually reject

A

fact

226
Q

what are the 4 types of rejection

A

Hyperacute
accelerated
acute
chronic

227
Q

what is responsible for the hyperacute rejection

A

complement activated

within hours

228
Q

what is responsible for the accelerated rejection

A

within days

memory T cells

229
Q

what is responsible for the acute rejection

A

days- weeks

primary response of T cells

230
Q

what is responsible for the chronic rejection

A

unknown cause

immune complex, recurrence of disease

231
Q

how do immunosuppressive drugs such as cyclosporine

tacrobimus and rapamycin work

A 
affect TCR MHC recognition
normal TCR signalling
transcription of IL2 feeds back to TOR (target of rapamycin) IL2 R activated TOR
Rapamycin- blocks IL2 production
T cells cant be stimulated
232
Q

what is the alpha gal problem

A

2 linked galactose sugars on pig cell surface
gal alpha 1 3 gal
present on many microbes- lots of IgG against them
KO alpha gal- no rejection

233
Q

what are the two forms of immuno deficiency

A

primary-genetic

secondary-effect of external agent

234
Q

in what age group is primary ID more common

A

children

235
Q

how could a mutation have an effect on a protein

A

stop codon- truncated protein

point mutation- misfolding

236
Q

give 3 examples of primary immunodeficiency affecting the innate immune system

A

Chronic granulomatous disease-
leukocyte adhesion deficiency- ß2 integrin defect affecting neutrophils and monocytes

Complement deficiencies- most profound in C3 as all pathways meet here
-C8- no membrane attack complex

237
Q

chronic granulomatous disease

A

Nadp oxidase defect affects phagocytic cell- cant produce respirative burst- the release of reactive oxygen species

NADPH oxidase makes super oxide (02 -)
NADPH oxidase made up of
P22phox transmembrane
gp91phox- transmembrane- x chromosome
p47phox
p67phox
rac2
p40phox

gp91phox x chromosome more likely in men

238
Q

Primary immunodeficiency affecting adaptive immune response

A

B-cell:

  • selective IgA deficiency
  • Hyper-IgM syndrome
  • X- linked agammaglobulinaemia- Bruton’s tyrosine kinase

T-cell:
Wiskott-Aldrich syndromeWASP
DiGeorge syndrome TBX1

severe combined immunodeficiency

239
Q

Hyper IgM

A 
CD40 L defect
no class switching as there is no contact between Th and B cell
240
Q

selective IgA deficiency

A

1 in 300
most people dont even realised
covered up by other classes IgM taken to mucosal surface by poly Ig transporter

241
Q

severe combined immunodeficiency

A

RAG1/2

involved in recombination

242
Q

DiGeorge

A

in mice- nude
Tbx1
no T cells- recurrent infection
partially developed Thymus

243
Q

T- B- NK+ SCID

A

RAG1/2 15%
no T cells so B cells cant produce antibodies

Artemis 15%

244
Q

T- B+ NK-

A

gamma c Chain

JAK-3 10%

245
Q

T- B+ NK+

A

IL-7 R alpha

246
Q

causes of secondary ID

A

malnutrition- lack of calories, lack of iron/zinc

loss of cells or molecules of immune system through intestine in intestinal Lympangiectasia
nephrotic syndrome

Tumours of immune system- lymphoma, leukemia

cytotoxic drugs/irradiation- affects rapidly dividing cells

infection- malaria

247
Q

how does HIV work

A

hiv injects CD4+ cells that bind to it (MHC 2, professional antigen presenting cell Th2, macrophage)
CD4 + chemokine coreceptor (CCR5 in macrophage, CXCR4 in T cells)

gp120 binds to CD4. gp120 changes conformation. co recepto binds induces another conformational change which results in the movement of CD4 away and the binding of gp 41 which mediates fusion of HIV and cell through the fusion pore

248
Q

opportunistic infections

A

Virus cytomegalovirus
bacteria- mycobacterim tuberculosis
funghi pneumocystis jiroveci
protozoa toxoplasma gondii

249
Q

treatment of immunodeficiency

A

Antibiotics
gamma globulins- Ab for Ab deficiency
cell replacement- hematopoetic stem cell
gene therapy- take out defective gene

250
Q

what principles do vaccines utilise

A

Memory

specificity

251
Q

what is injected

A

Toxoid- non toxic modified toxin with many of the same epitopes

252
Q

what effectors are activated

A

Tc cells
antibody
Th

253
Q

what is an attenuated organism

A

an organism that is alive but not capable of causing disease

254
Q

what does an adjuvant do

A

stimulates dc so that they can activate T cells

mimicks PAMPs

255
Q

how does a carrier help

A

has similar epitope to toxoid

256
Q

what does a vaccine have to be?

A 
effective
available
safe
stable 
affordable
257
Q

what does a vaccine consist of

A

Antigen
carrier
adjuvant

258
Q

smallpox

A

wiped out in 1979

work started 1798

259
Q

rinderpest

A

wiped out in cattle in 2011

260
Q

what were the two types of vaccines used for polio

A

Salk- inactivated 1956

Sabin-attenuated mid 1960s

261
Q

what were the problems with wiping polio out?

A

hard to target the IgA response
oral drops administered- IgA rises in mucous of lungs and nasl butharder to raise intramuscular IgA

hard to reach some areas of the world e.g afghanistan- war zone

262
Q

what is antigenic shift

A

exchanges of genome between human avian and swine version of bacteria

263
Q

what is antigenic drift

A

point mutations changes genome

264
Q

why do you need a new influenza jab every year

A

lots of shift and drift

peoples job around the world to find the most likely next flu bout
done 2 times a year for both hemispheres

265
Q

problems with HIV vaccines

A

identification of Immunogens
and immunisation stratergy

broad and long lasting CTL immunity
broadly neutralising antibodies

266
Q

where has there been a small break through in HIV vaccine

A

Thailand
4 infections of recombinant canarypox vector with HIV gag, pol, env genes
2 booster injection

limited protective efficacy

267
Q

where has there been a small break through in HIV vaccine

A

South africa

tried the Thai vaccine - similar response

268
Q

malaria

A

trial in children between 5 and 17 months 50% protective

269
Q

why are conjugate vaccines used

A

cojugate vacine = polysaccharide+ protein
polysaccharide would produce T independent response, adding protein get T dependent one

example
meningococcus group C

270
Q

who are vaccines given to

A

‘at risk’ groups
BCG (TB) under 35

Chickenpox- any age

flu- children/elderly

Pneumococcal vaccine( 2-65)
Hep B- birth onwards
271
Q

why is yellow fever the holy grail of vaccines

A

1 shot- lifetime immunity

272
Q

why is a gene gun used

A

injects genes/ proteins into arm

gene expressed- activates Tc cells- mimicks immune response

273
Q

what are the potential mechanisms for immune system attacking tumours

A

antibody + complement
antibody dependent cytotoxicity eosiniphils
direct NK cytotoxicity
Tc recognising tumour derived peptides

274
Q

what are the problems with using the immune system to attack tumours

A

tumours express our protein- dont have different MHC etc

275
Q

is there a link between virus and tumours

A

yes some tumours are caused by viruses

primary ID more likely to develop lymphome- EBV

immunosuppression- lymphoma-EBV
cervical cancer HPV
skin papilloma
liver Hep b + c
Kaposi's sarcoma- human herpes

malaria Burkitts lymphoma EBV

276
Q

EBV can cause

A

Lymphoma- ID/IS

Burkitt’s lymphoma- Malaria

277
Q

micro organisms and cancer

A

helicobacter pylori- stomach cancer

most not caused by viruses

278
Q

what causes most cases of cancer

A

multiple mutations

p53 mutation causes tumour specific antigens in colorectal, lung, bladder, head ad neck

279
Q

developmental tumour

A

usually developmental proteins
MAGE- melanoma associated gene
causes melanoma, colorectal, lung and gastric tumours

280
Q

viral antigens

A

antigens from tumour expressed by virus
HPV
cervical

281
Q

tumour associated

A

not just in tumours also in other cells. present in tumour in higher numbers
PSA
prostate

282
Q

overexpressed

A

very high levels on tumour some on normal cells
her 2
breast cancer

283
Q

why doesnt the immune system attack tumours

A

tumours have mechanisms that prevent attack

clonal selection of cells that do not express tumours- has a survival advantage

secrete molecules to down regulate dendritic cells

down regulate cytotoxic T lymphocytes

Treg stimulated

284
Q

how do tumours down regulate DCs

A

T cells need CD 80 86 stimulation simultaneously to activate
PRRs recognise pamps and damps in infection which upregulates CD80 86 on DCs

tumours do not release Pamps and DAMPs

ANERGY

285
Q

how do tumours immunosuppress

A

VEGF
IL10
are both immunosuppressive

TGF ß- normally from Treg

Tregs usually tumour infiltrating- suppress immune system

286
Q

why has tumour specific or associated proteins not been successfull

A

Tregs prevent it from killing tumour

does increase immune response

287
Q

what potential immunotherapies for tumour

A

Antibody
cell transfer
vaccine

288
Q

antibody

A

recognise antigen specific or associated activates complement/killer cells

could attach toxin to antibody (only TSA)

289
Q

T cell transfer

A

take out from patient increase number of T cells and replace

grow dendritic cells
use GMCSF IL4 drive monocyte to DC

tumour antigen and cytokine taken into DC

cytokine helps DC mature
DCs infused into patient present tumour antigen to T cells

290
Q

vaccine

A

immunise against virus

therapeutic
Induce Tc cell response

IMMN2001 (1 decks)

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