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π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž > Generation of Diversity in the T cell Repertoire > Flashcards

Generation of Diversity in the T cell Repertoire Flashcards

1
Q

What is an antigen?

A

➝ a molecule that can bind specifically to an antibody

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2
Q

What do adaptive immune reactions occur to?

A

➝ specific epitopes not the whole antigen

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3
Q

What is an epitope?

A

➝ A small portion of an antigen

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4
Q

What are epitopes a target for?

A

➝ TCR, antibodies and MHC

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5
Q

How many epitopes can one antigen have?

A

➝ Multiple

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6
Q

What do infection and vaccination induce?

A

➝ polyclonal T and B cell responses

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7
Q

What is the key difference between B cells and T cells?

A

➝ B cells recognise whole antigens and process them

➝ T cells don’t recognise native antigens

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8
Q

What happens when a B cell recognises a whole antigen?

A

➝ It receives additional activation signals
➝ the B cell proliferates and produces clones
➝ they all produce antibodies that are identical to the original B cell

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9
Q

How can T cells recognise antigens?

A

➝ The antigens must be processed for T cells to recognise them

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10
Q

What happens to the peptides that an antigen generates?

A

➝ they can be presented on the surface of an APC

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11
Q

What does a T cell need to do to be activated?

A

➝ interact with an antigen presenting cell to be active

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12
Q

What forms of an antigen will a T cell NOT have a response to?

A

➝ soluble native Ag
➝ cell surface native Ag
➝ Soluble peptides of Ag
➝ cell surface peptides of Ag

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13
Q

What form of antigen will a T cell have a response to?

A

➝ Cell surface peptides of Ag presented by cells that express MHC antigens

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14
Q

What types of APC will cause a T cell response and why?

A

➝ live APCs

➝ there are additional signals that only viable cells produce that can activate T cells

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15
Q

What are the 5 ways that exogenous antigens can be taken up?

A 
➝ Phagocytosis 
➝ pinocytosis 
➝ Fc receptor mediated phagocytosis 
➝ complement receptor mediated phagocytosis 
➝ membrane Ig receptor mediated uptake
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16
Q

Which 4 immune cells recognise and process antigens?

A

➝ Monocytes
➝ Dendritic cells
➝ B cells
➝ macrophages

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17
Q

What are the main APCs?

A

➝ myeloid cells

➝ monocytes and macrophages

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18
Q

What is the most advanced type of APC?

A

➝ Dendritic cells

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19
Q

What is the difference between macrophages and monocytes?

A

➝ monocytes are blood circulating cells

➝ macrophages are in tissues and are terminally differentiated monocytes

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20
Q

What two cell types can monocytes become?

A

➝ dendritic cells or macrophages

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21
Q

Where are dendritic cells found?

A

➝ mucosal tissues

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22
Q

What do dendritic cells induce?

A

➝ strong T cell responses and inflammation

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23
Q

What are macrophages better at doing than dendritic cells?

A

➝ better equipped to kill pathogens

➝ NO production

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24
Q

What are dendritic cells better at doing than macrophages?

A

➝ migrating to lymph nodes via CCR7 and presenting antigens to T cells

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25
Q

Where are B cells highly abundant?

A

➝ In mucosal tissues

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26
Q

How do B cells internalise antigens?

A

➝ receptor mediated internalisation

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27
Q

What is the primary function of B cells?

A

➝ to make antibodies but they are still good at antigen presentation

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28
Q

What bacterium are dendritic cells important against?

A

➝ Mycobacterium tuberculosis

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29
Q

What cell is the main inducer of the T cell immune response to neisseria meningitidis?

A

➝ B cells

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30
Q

What are the 4 steps for endogenous antigen processing?

A

➝ Uptake
➝ degradation
➝ antigen-MHC complex formation
➝ Presentation

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31
Q

When is endogenous antigen uptake done?

A

➝ when the antigens/pathogens are already in the cell

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32
Q

What is endogenous antigen degradation?

A

➝ Pathogenic antigens synthesised in the cytoplasm undergo limited proteolytic degradation in the cytoplasm

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33
Q

What is the antigen-MHC complex formation?

A

➝ loading of the peptide antigens onto MHC class I molecules

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34
Q

What is presentation of endogenous antigens?

A

➝ transport and expression of antigen MHC complexes on the surface of cells for recognition by T cells

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35
Q

What are macrophages specialised for?

A

➝ motility, phagocytosis and the introduction of particles to the lysosomal system

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36
Q

Why is a non-lyosomal mechanism to process antigens necessary?

A

➝ most cell types do not have lysosomal systems but viruses can infect most cell types

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37
Q

How does cytosolic presentation occur?

A

➝ The viral protein is in the cytosol
➝ It enters the proteasome
➝ It is cleaved into multiple peptides
➝ loaded onto MHC class I and presented on the cell surface

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38
Q

How are antigens from inactive viruses processed?

A

➝ via the exogenous pathway

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39
Q

What kind of a response do inactive viruses raise?

A

➝ a weak cytotoxic response

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40
Q

What kind of drugs is the processing of antigens from inactive viruses sensitive to?

A

➝ lysosomotropic drugs

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41
Q

What is required for non-lysosomal antigen processing?

A

➝ protein synthesis

42
Q

How are antigens from infectious viruses processed?

A

➝ via the endogenous pathway

43
Q

Describe the endogenous pathway/Class I pathway?

A

➝ The antigen is processed
➝ it is cleaved into multiple peptides
➝ presented on the MHC class I on the surfaces
➝ MHC I activates a CD8 cell

44
Q

Describe the endosomal pathway?

A

➝ Antigens are endocytosed by macrophages
➝ They are sequestered to lysosomes or endosomes
➝ Processed in the lysosomes and loaded onto MHC II molecules within the lysosomes
➝ MHC II activates a CD4 T cell

45
Q

Where are Exogenous pathogens directed?

A

➝ MHC II

46
Q

Where are Endogenous pathogens directed?

A

➝ MHC I

47
Q

How are exogenous pathogens eliminated?

A

➝ Antibodies and phagocyte activation by T helper cells that use antigens generated by exogenous processing

48
Q

How are endogenous pathogens eliminated?

A

➝ Killing of infected cells by CTL that use antigens generated by endogenous processing

49
Q

Where is MHC I expressed?

A

➝ all nucleated cells

50
Q

Where is MHC II expressed?

A

➝ on APCs and activated T cells

51
Q

What does MHC I bind to?

A

➝ short peptides

➝ 8-10 amino acids

52
Q

What does MHC II bind to?

A

➝ long peptides

➝ 15-24 amino acids

53
Q

What does MHC I present to?

A

➝ CD8+ T cells

54
Q

What does MHC II present to?

A

➝ CD4+ T cells

55
Q

Where does MHC I get its antigens from?

A

➝ from the cytosol

56
Q

Where does MHC II get its antigens from?

A

➝ Phagosomes and endosomes

57
Q

How many MHC class I isotypes are there?

A

➝ 6

58
Q

How many MHC class II isotypes are there?

A

➝ 5

59
Q

What are the similarities between TCR and BCR?

A

➝ Belongs to Ig superfamily
➝ Like Fab fragment of antibody
➝ large diversity
➝ single specificity

60
Q

What are the differences between TCR and BCR?

A

➝ Lower affinity
➝ cannot be released
➝ no Fc fragment so no cellular functions
➝ single binding site not two
➝BCR has 5 classes
➝ TCR has 2 classes alpha beta and delta gamma

61
Q

What are the two mechanisms that generate BCR diversity?

A

➝ Before antigen stimulation : somatic recombination

➝ after antigen stimulation : somatic hypermutation

62
Q

What is the mechanism that generates TCR diversity?

A

➝ before antigen stimulation : somatic receombination

➝ after antigen stimulation : none

63
Q

When does receptor gene rearrangement take place?

A

➝ during T cell development in the thymus

64
Q

What is the three signal mode of activation for T cells?

A

1) peptide-MHC (pMHC)
2) Co-stimulation
3) Cytokines

65
Q

What is the third signal important for when activating T cells?

A

➝ amplification of the response and determining T cell phenotype

66
Q

How is the peptide-MHC signal delivered to the T cell ?

A

➝ The main signal (1) is delivered from the APC by a peptide-MHC complex to the TCR

67
Q

How is the co-stimulatory signal delivered to the T cell?

A

➝The co-stimulatory signal (2) is delivered from the APC by germline-encoded accessory receptors such as the B7 family (CD80 and CD86)

68
Q

What type of T cell does IL-12 promote?

A

➝TH1 cells

69
Q

What type of T cell does IL-4 promote?

A

➝TH2 cells

70
Q

What type of T cell does IL-23 promote?

A

➝TH17 cells

71
Q

What is the immunological synapse?

A

➝ signals 1 and 2 are central

➝ surrounding integrins and accessory molecules help to stabilise the interaction

72
Q

What is the central interaction in the immunological synapse?

A

➝ T cell and peptide-MHC complex

73
Q

What is the central interaction like in the immunological synapse?

A

➝ short lived and has a low affinity

74
Q

What are the co-stimulatory molecules that promote T cell binding and what do they interact with?

A

➝ CD80/CD86 or B71 and B72 interacting with the T cell partners CD28 and CTLA4

75
Q

What is the function of the co-stimulatory molecules?

A

➝ They strengthen the activation of the two cells and provide additional signals for the activation of the T cells

76
Q

What is the function of integrins during T cell binding?

A

➝ keep the cells in contact

77
Q

What are the pathways used in peptide-MHC binding to TCR and what is the effect?

A

➝ Lck
➝ Zap70
➝ PLC- gamma
➝ effect : calcium flux & NFAT activation

78
Q

What are the pathways used in co-stimulation and what is their effect?

A

➝ PI3K
➝ Akt
➝ MAPK
➝ effect : NF- kappa B activation

79
Q

How are T cell co-receptors expressed?

A

➝ co-expressed with the TCR

80
Q

How many co-receptors do the T cells have?

A

➝ one

81
Q

What do CD4 cells do?

A

➝ help other cell types by secreting cytokines

82
Q

What do CD8 cells do?

A

➝ kill infected cells directly

83
Q

What do TH1 cells do?

A

➝ produce cytokines which will activate macrophages and the macrophages will kill intracellular pathogens more efficiently

84
Q

What do TH2 cells do?

A

➝ Produces other cytokines which activate B cells and the B cells will then produce antibodies and neutralise circulating viruses and prevent colonisation of bacteria

85
Q

What do negative regulators of antigen presentation do?

A

➝ provide an immune checkpoint to limit T cell activation

86
Q

What are the two important molecules in T cell regulation?

A

➝ CTLA4 (cytotoxic T lymphocyte associated protein)

➝ PD-L1 (programmed death ligand 1)

87
Q

Describe how PD-L1 and CTLA-4 work to inhibit T cell function?

A

1)The T cell receptor interacts with APCs which leads to T cell activation
2)PD-1 is expressed on T cells
If it is activated by PD-L1 (ligand) it leads to a blockade of T cell receptor activation
3)This is through multiple signalling pathways
4)CTLA-4 acts on the co-stimulatory molecules (both signal 1 and 2 are important for T cell activation)
5)Both signals can be blocked with CDLA-4

88
Q

What is positive selection in the thymus?

A

➝ T cells that can’t bind self antigen-MHC are deleted

➝ these cells are useless because they won’t protect against pathogens

89
Q

What is negative selection in the thymus?

A

➝ T cells that bind self antigen-MHC too strongly are also deleted
➝ these cells are dangerous because they are too self reactive

90
Q

What is the stochastic model?

A

➝ A proportion of T cells that are strongly reactive to self-antigen will express the transcription factor FOXP3 which is the β€˜master controller of regulatory T cells

91
Q

What can Treg cells do?

A

➝ they can compete with any autoreactive T cells and secrete anti-inflammatory cytokines

92
Q

What are Treg cells also called?

A

➝ CD25

93
Q

What do Treg cells secrete?

A

➝ interleukin 10 and TGF beta

94
Q

What are obligate parasites?

A

➝ organisms that depend on the human host for survival

95
Q

How does mycobacterium tuberculosis evade the immune system?

A 
➝ Upregulated PD-L1 on APCs to shut down T cell activation
➝ Blocks MHC class II expression
96
Q

How does neisseria meningitidis evade the immune system?

A 
➝ Blocks DC activation which decreases CD40, CD86 and MHC class I and II expression
➝ Antigens are homologous to self-antigens so anergic T cells
97
Q

How does Neisseria gonorrhoea evade the immune system?

A

➝ It expresses Opa protein which binds to.T cells and induces tyrosine phosphatases that β€˜switch off’ key molecules involved in TCR signalling

98
Q

How does HIV evade the immune system?

A

➝ Upregulates PD-1 on T cells which antagonises TCR signalling
➝ Binds to DC-SIGN to suppress DC activation via Rho-GTPases

99
Q

How does HSV evade the immune system?

A

➝ Produces protein which binds to and inhibits TAP

➝ prevents viral peptide transfer to the ER

100
Q

How does adenovirus evade the immune system?

A 
➝ Produces protein which binds MHC class I molecule 
➝ prevents MHC class I from leaving the ER

π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž (14 decks)

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