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Year 3 > Advanced Immunology > Flashcards

Advanced Immunology Flashcards

1
Q

Proteasome

A

Splices peptides into readable fragments for antigen presentation.

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2
Q

TAP

A

Transports short peptides produced by the proteasome into the rough E.R lumen.

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3
Q

B1i, B2i and B5i

A

Sections of the proteasome that are found within the immunoproteasome form. They replace the B1,B2 and B5 cells within the constitutive proteasome.

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4
Q

Tapasin

A

Keeps empty MHC I molecules in the endoplasmic reticulum until they receive their peptide.
Promotes assembly of MHC I with peptides.

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5
Q

What is crucial for tapasin function?

A

Formation of disulphide-linked conjugates of tapasin with ERp57.

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6
Q

TLR role

A

Recognise pathogen-associated molecular patterns from exogenous sources or cell surfaces which induces dimerisation and thus, signalling occurs.

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7
Q

What does TLR signalling lead to?

A

Expression of Pro-inflammatory Cytokines

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8
Q

What do TLRs located on the cell surface of an APC detect?

A

Extracellular pathogens

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9
Q

What do TLRs located within the endosome membrane recognise?

A

Pathogenic/ foreign molecules digested and broken down by endosomic enzymes.

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10
Q

What are Mannose receptors and Scavenger receptors?

A

Pattern recognition receptors, they recognise PAMPs

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11
Q

Summarise the endocytic pathway of MHC class 2 presentation

A
  • Antigen is taken up from the extracellular space and into endocytic vesicles.
  • Acidification of the vesicles activates protease to degrade antigen into peptide fragments.
  • Vesicles containing peptides fuse with vesicles containing MHC Class II molecules.
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12
Q

What is the method of MHC Class 2 presentation known as?

A

Endocytic

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13
Q

What is the method of MHC Class I presentation known as?

A

Cytosolic

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14
Q

How does mouse herpes virus protein target newly synthesized MHC class I molecules?

A

By adding ubiquitin to the cytoplasmic tail of MHC I. This directs the new MHC from the E.R to the proteasome in the cytosol for complete destruction.

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15
Q

DRiPs

A

Defective Ribosomal products
- Includes unusable products translated from the mRNA which appear in the cytoplasm and can be both self and pathogen derived proteins.

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16
Q

How are DRiPs disposed of?

A

They are recognised and tagged by ubiquitin for rapid destruction by the proteasome.

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17
Q

ERAAP

A

Endoplasmic reticulum aminopeptidase. Trims the amino-terminus of peptides if they are too long so they fit better into the MHC Class I groove.

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18
Q

What is ERAAP expression upregulated by?

A

The presence of IFN-y.

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19
Q

What must a MHC Class I molecule associate with first, prior to the peptide?

A

Beta2-microglobulin

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20
Q

Which MHC is presented on professional antigen-presenting cells?

A

Class 2

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21
Q

Which MHC is presented on all nucleated cells?

A

Class 1

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22
Q

What sort of protein is degraded the most by the proteasome?

A

DRiPs

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23
Q

What is the protein loading complex comprised of?

A

Calreticulum, ERp57, Tapasin, TAP and MHC I

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24
Q

How is the Protein loading complex formed?

A

Calnexin binds to B2M.

MHC I is released from Calnexin

MHC I then binds to the chaperone proteins (Calreticulum, ERp57)

This then binds to TAP via Tapasin.

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25
Q

What is PA28

A

Doorkeeper/activator of the proteasome.
Must bind to both ends of the proteasome for it to activate.

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26
Q

What are the chaperone proteins that assist within the protein loading complex?

A

Calreticulum, Tapasin and ERp57

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27
Q

Summarise the Cytosolic pathway of antigen presentation

A

Proteasome processes proteins into peptides

Peptides are transported by TAP1 and TAP2 to the E.R

Peptides associate with MHC I heavy chain (after calnexin has bound B2M) Tapasin assists this

Tapasin then allows MHC/Peptide complex to leave E.R

This is then transported to the surface for CD8 T cell inspection

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28
Q

At which pH does the invariant chain break down to form CLIP?

A

5

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29
Q

What does HLA-DM do?

A

Aids MHC folding but also checks for weakly bound or unstably bound antigenic peptides attached to MHC II.

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30
Q

How does HLA-DM prevent poorly bound peptides?

A

It will bind to the peptide/MHC II complex and remove the peptide.

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31
Q

What does the removal of poorly bound peptides allow?

A

A method of peptide editing. Makes presentation more accurate as peptides can be displayed for days upon APCs

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32
Q

What increases expression levels of HLA-DM?

A

IFN-y

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33
Q

What makes up the invariant chain/Class II MHC complex?

A

3 x MHC II molecules
3 x Invariant chains

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34
Q

What does the invariant chain leave in the groove of MHC II?

A

CLIP, a small fragment.

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35
Q

What is contained in the cytoplasmic tail of the invariant chain and what does it do?

A

Sorting signals that direct the transport of MHC II from the E.R to the trans-Golgi then towards the acidified late endosome.

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36
Q

What does Milatuzumab do?

A

Bind to CD74 and is used to treat some cancers which express this protein.

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37
Q

Where is MARCH-1 found?

A

In recycling endosomes

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38
Q

What does MARCH-1 do?

A

Ubiquitinates MHC molecules in immature dendritic cells, targeting them for degradation when there is no foriegn antigen.

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39
Q

What switches off the production of MARCH-1?

A

Crosslinking/dimerisation of TLR when a foriegn antigenic fragment is sensed.

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40
Q

Why is MARCH-1 turned off in the presence of an antigen?

A

Cell is dealing with pathogens so would be counter-productive to destroy the MHC molecules. Allows MHC to transport to the cell surface.

41
Q

Where is high variation seen in MHC I molecules?

A

Alpha 1 and alpha 2 regions

42
Q

Where is high variation seen in MHC II molecules?

A

Beta 1 region

43
Q

How fast is the kinetics for MHC/Peptide binding?

A

Slow, stability allows accumulation and persistence of MHC/foriegn peptide complexes on the cell surface of the APC to allow recognition by T cells.

44
Q

How fast is the kinetics for TcR/MHC binding?

A

Fast, disassociation rate allows several triggering events of many TcRs in seconds rather than hours or days for allowing rapid T cell activation.

45
Q

What is signal 1 involved in the activation of naive T cells?

A
  • Binding of MHC II to TCR mediated by CD4
46
Q

What is signal 2 involved in the activation of naive T cells?

A
  • Costimulation, B7 of APC binds to CD28. This must happen for continued survival of the cell.
47
Q

What is signal 3 involved in the activation of naive T cells?

A
  • From cytokines (mostly pro-inflammatory) coming from APCs, binding to receptors on the T cell and finally the T cell differentiates.
48
Q

What does IL23 do?

A

Differentiates T cells into T helper 1 cells which help CD8 cytotoxic T cells.

49
Q

What does IL-4 do?

A

Differentiates T cells into T helper 2 cells which help B cells.

50
Q

What does IL-6 do?

A

Induces T cell differentiation

51
Q

What is anergy?

A

State of a T cell which has been completely turned off and cannot be restimulated.

52
Q

Can T cells recieve signal 1 from self cells?

A

No, this is the cause of autoimmunity and should not happen.

53
Q

What is the role of the invariant chain?

A

Blocks accidental MHC cytosolic binding. Prevents peptides already in the cytosol/E.R from binding by mistake.

54
Q

What would happen in the TcR affinity for MHC/peptide was very high?

A

Wouldn’t get a lot of activation events.

55
Q

What is peptide editing?

A

Use of HLA-DM binding to peptide-MHC II complexes allows peptides of higher affinity to bind at a higher stability.

56
Q

Why is peptide editing needed?

A

MHC II/peptide complex must persist at surface of APC for many days = needs to be stable.

57
Q

What increases the expression of HLA-DM

A

IFN-y

58
Q

When is it useful to block costimulation?

A

Transplants, to prevent rejection
Autoimmunity, switching off autoimmune responses

59
Q

What is a Langerhans cell?

A

Highly immature DC cell

60
Q

Which 3 cells are able to take up antigen?

A

Dendritic cells, Macrophages and B cells

61
Q

How do Dendritic cells take up antigen?

A

Macropinocytosis and Phagocytosis

62
Q

How do Macrophages take up antigen?

A

Macropinocytosis and Phagocytosis

63
Q

How do B cells take up antigen?

A

Antigen-specific receptor

64
Q

How do DCs present viral antigens even when they’re not infected?

A

Via cross-presentation, allows viral peptides to enter cytosol.

65
Q

What is cross-presentation?

A

Method of presenting viral peptides on MHC I to CD8 T cells.

66
Q

What molecule assists transportation across the endosomal membrane into the cytosol for cross-presentation?

A

Sec61

67
Q

What is Sec61?

A

ATP-dependent transporter/translocon

68
Q

What allows Sec61 to leave the E.R to reach individual endosomes for transportation?

A

TRIF signalling

69
Q

What initiates TRIF signalling?

A

TLRs

70
Q

Process of TRIF mediated transport

A

TLRs detect viral proteins
Initiates TRIF signaling
Allows Sec61 to move from E.R to enter endosomal membrane to allow transport

71
Q

What is Autophagy?

A

The reverse of cross-presentation.
Cytoplasmic material is cannibalised by specialized vesicles (autophagosomes) which then fuse with lysosomes that degrade proteins into peptides.

72
Q

Why do cells deploy autophagy?

A

It is a method of getting protein aggregates/whole foreign microorganisms from within the cell but are too big to be degraded by the proteasome

73
Q

What induces autophagy?

A

TLRs, NOD-like receptors, DAMPs, IFN-y, TNF-a

74
Q

What happens once DCs mature?

A

Express heightened levels of B7, MHCI and MHCII and a number of adhesion molecules.

75
Q

Which chemokine receptor hones DCs to lymph nodes?

A

CCR7

76
Q

What type of cells do not always need to recieve signal 2 of costimulation to survive?

A

Effector B and T cells

77
Q

What does transfection of tumour cells with GM-CSF gene allow?

A

Increased production of GM-CSF for activation of neighboring DC cells.
Allows presentation of tumour antigens upon DCs and costimulation to both Th cells and CTL precursors.

78
Q

What are the MHC I classes in humans?

A

A,B and C - hereditary

79
Q

What are the MHC II classes in humans?

A

DP,DQ,DR - affects immunological susceptibility

80
Q

What are the MHC III classes in humans?

A

C4,C2 and BF –> nothing to do with histocompatibility

81
Q

Autograft

A

From one part of the body to another.
E.g trunk to arm

82
Q

Isograft

A

Between genetically identical individuals.
E.g monozygotic twins

83
Q

Allografts

A

Between different members of the same species
e.g Mr Smith to Mr Jones

84
Q

Xenografts

A

Between members of different species.
e.g monkey to man

85
Q

Which types of graft are usually accepted?

A

Autografts and Isografts

86
Q

Which grafts are accepted with immunosuppression?

A

Allografts

87
Q

THE LAWS OF TRANSPLANTATION OF SKIN GRAFTS (INBRED MICE)
Inbred mice - skin transplant onto exactly the same mouse

A

ACCEPTED

88
Q

THE LAWS OF TRANSPLANTATION OF SKIN GRAFTS (INBRED MICE)
Brown mouse onto grey

A

Skin recognised as foriegn = REJECTED

89
Q

THE LAWS OF TRANSPLANTATION OF SKIN GRAFTS (INBRED MICE)
Brown mouse onto offspring AxB

A

ACCEPTED –> not technically foreign

90
Q

THE LAWS OF TRANSPLANTATION OF SKIN GRAFTS (INBRED MICE)
AxB onto brown mouse

A

REJECTION –> never seen AxB antigen before

91
Q

Steps of graft acceptance

A
  1. Revascularisation days 3-7
  2. Healing days 7-10
  3. Resolution days 12-14
92
Q

Steps of First set rejection

A
  1. Revascularisation days 3-7
  2. Cellular infiltration days 7- 10
  3. Thrombosis and necrosis CLOT FORMATION days 10-14
93
Q

Steps of second set rejection

A
  1. Cellular infiltration days 3-4
  2. Thrombosis and Necrosis days 5-6
94
Q

What are minor HLA antigens?

A

Antigens that can cause some graft rejection. Minor HLA antigens can cause slow rejection of grafts even between members of MHC-identical mouse strains

95
Q

How are alloantigens in grafted organs recognized?

A

Via direct and indirect recognition

96
Q

Direct allorecognition

A

Recognition of donor graft antigens (peptide and foreign MHC) on the surfaces of donor APCs that have migrated to recipient LN.

97
Q

Indirect allorecognition

A

Recognition of processed and presented donor antigenic peptides on recipient APCs for presentation within the LN.

98
Q

What chemokines are required for CD8 T cell activation

A

IL-2 and IFN-y

99
Q

What chemokines are required for B cell activation?

A

IL-2, IL-4 and IL-5

Year 3 (4 decks)

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