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PMCOL 344 > Immune-8 > Flashcards

Immune-8 Flashcards

1
Q

what 2 things characterize cancer

A
  • accumulation of genetic alterations

- loss of normal cellular regulatory processes

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2
Q

what is 1 consequence of cancer (cellular)

A

expression of different antigens

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3
Q

what does cancer lead to (cellularly)

A

presentation of peptides bound to MHC 1 molecules on surface of cancer cells

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4
Q

what is a way that you can distinguish normal cells and cancer cells

A

presentation of peptides bound to MHC 1 molecules on surface of cancer cells

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5
Q

what are 3 types of tumor antigens

A
  • mutational antigens (neoantigens)
  • tumor associated antigens
  • cancer/testis antigens
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6
Q

what is special about mutational antigens (neoantigens)

A

they are completely absent from normal host cells

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7
Q

what are mutational antigens (neoantigens) derived from

A

mutated self-proteins or oncogenic viral proteins

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8
Q

are there mutational antigens (neoantigens) in normal cells

A

no

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9
Q

are there tumor associated antigens in normal cells

A

very low levels

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10
Q

what are tumor associated antigens

A

nonmutated proteins overexpressed in cancer cells

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11
Q

what do tumor associated antigens result from

A

genetic amplification

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12
Q

are there cancer/testis antigens in normal cells

A

only in reproductive tissues

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13
Q

do all tumors express cancer/testis antigens

A

no only by various tumor types

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14
Q

what happens after cancer releases antigens

A

cancer antigen presentation by APCs

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15
Q

what causes cancer to release antigens

A

often cell death

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16
Q

what happens once cancer antigens are presented by APCs

A

it causes T cells to rush to the tumor and infiltrate

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17
Q

what happens once T cells recognize cancer ells

A

they kill them

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18
Q

what must occur at the same time as tumor antigen presenting

A

cytokine release

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19
Q

what are 3 examples of cancer-immune cycle not working

A
  • tumor antigens may not be detected
  • T and DCs cells may not treat antigens as foreign
  • T cells may not get to and into the tumors
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20
Q

what is the role of cancer microenvironment

A

suppresses effector T cells

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21
Q

what is the main goal of cancer immunotherapy

A

initiate or reinitiate a self sustaining cycle of cancer immunity

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22
Q

what may be a downside of cancer immunotherapy

A

unwanted damage to normal cells and tissues, autoimmune

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23
Q

what are 3 sites for therapeutic intervention

A
  • promoting antigen presentation functions of DC
  • promote protective T cell responses
  • overcoming immunosuppression in the tumor
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24
Q

how do you promoting antigen presentation functions of DC (1 word)

A

vaccines

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25
Q

how do you promote protective T cell responses

A

engineering T cells (CAR T cells)

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26
Q

how do you overcoming immunosuppression in the tumor

A

checkpoint blockers

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27
Q

what is vaccination

A

administration of an antigen to produce immunity to a disease

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28
Q

what is cancer vaccines

A

formulation of TAs able to elicit an immune response to arrest the progression of cancer and prevent it from recurring

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29
Q

what do cancer vaccines induce

A

specific and long lasting lasting immune response against TA

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30
Q

what do classical vaccines rely on

A

random encounter of the vaccine with host DCs

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31
Q

what are DNA vaccines

A

naked DNA plasmids designed to deliver genes encoding tumor antigens

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32
Q

how are the DNA plasmids engineered in DNA vaccines

A

to include genes coding for co stimulatory molecules (Cyokines)

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33
Q

what happens to the antigen encoded by DNA vaccine

A

it is expressed and presented on MHC molecules

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34
Q

which MHC molecules are antigens presented on with DNA vaccines

A

both 1 and 2

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35
Q

which T cells are activated with DNA vaccines

A

CD4 and CD8 t cells

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36
Q

do DNA vaccines activate innate immunity

A

yes

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37
Q

what do they inject with cell based tumor cell vaccines (older ones)

A

whole tumor cells or cell lysates of allogenic source

38
Q

what do they inject with cell based tumor cell vaccines (newer ones)

A

autologous tumor material

39
Q

what are tumor cells co injected with in cell based tumor cell vaccines + why

A

adjuvant and/or cytokines or growth factors to increase immunogenicity

40
Q

how are tumor cells engineered in cell based tumor cell vaccines

A

to express immunostimulatory cytokines or co-stimulatory molecules

41
Q

what do they culture from blood in DC vaccines

A

monocytes

42
Q

what do they load immature DCs with in DC vaccines + why

A

with antigens so they mature

43
Q

what do they do to the monocytes they extract from blood in DC vaccines

A

they are cultured with various cytokines to produce immature DCs

44
Q

what do they reinfuse back into the patient in DC vaccines

A

mature DCs

45
Q

what do DC vaccines induce in the human

A

antigen specific T and B cell responses

46
Q

where do they induce DC activation in DC vaccines

A

ex vivo

47
Q

what type of vaccine is DC vaccine

A

cell based

48
Q

what are the 2 types of cell based vaccines

A

tumor cell vaccines and DC vaccines

49
Q

what do they use in protein/peptide based vaccines

A

identified tumor antigens

50
Q

what are 3 types of tumor antigens used in protein based vaccines

A
  • whole TA (protein)
  • TA-derived peptides
  • synthetic peptides containing the neoantigen sequences
51
Q

what are antigens injected with in protein vaccines

A

adjuvant (boost immune ersponse)

52
Q

what happens to protein vaccines once they are in the body

A

captured by tissue resident DCs, presented with MHC 2 (maybe 1 too)

53
Q

how do recombinant viruses as vaccines work

A

the viruses are engineered to express a defined TA

54
Q

what are major advantages to recombinant viruses as vaccines work

A

strong immunogenicity which leads to significantly greater immune response

55
Q

what are major obstacles to recombinant viruses as vaccines work

A

presence of development of neutralizing antibodies against viral proteins

56
Q

what is special about oncolytic viruses

A

they only replicate in cancer cells, not in normal cells

57
Q

what do oncolytic viruses promote

A

anti tumor responses

58
Q

what is the 2 ways that oncolytic viruses can be used

A

in situ (inside the tumor) and systemic

59
Q

what does infection with oncolytic viruses cause

A

release of TAs and PAMPs and DAMPs

60
Q

how do oncolytic viruses kill cells

A

they enter cells, cause the release of TAs and PAMPs and DAMPs which then start the immune response

61
Q

how do personalized vaccines work (3 steps)

A

Take tumor sample from patient, do analysis of transcript, detect neoantigens/ tumor antigens that may be efficient to activate the immune system

62
Q

what are 2 T cell receptor targets used for cancer immunotherapy

A

TCR and CAR (chimeric antigen receptor)

63
Q

where do the TCRs come from for T cell cancer immunotherapy

A

responding patients

64
Q

where do the CARs come from for T cell cancer immunotherapy

A

synthesized from molecular biology techniques

65
Q

what is involved in T cell cancer immunotherapy with the TCR and CAR

A

insertion into T cells the receptors that can detect tumor antigens

66
Q

what are CAR T cells

A

T cells that express CARs

67
Q

what do CAR T cells recognize

A

tumor antigen directly on the surface of a tumor independently of MHC

68
Q

do CAR T cells use the MHC

A

no

69
Q

what is the structure difference of endogenous and engineered TCR

A

very similar

70
Q

what is the structure difference of endogenous and engineered CARs

A

they lack TCR chains

71
Q

what are the 2 things that make up CAR

A

antibody derived antigen recognition domain (extracellular, VL and VH) and intracellular T signalling stimulation domain

72
Q

what does the intracellular T signalling stimulation domain of CAR do

A

recruits endogenous downstream signalling molecules

73
Q

what do CAR T cells do (general + 3 specific)

A

provide tumor specific effector cells with enhanced functionality (superior cytotoxicity, persistence, antigen recognition)

74
Q

what does the antibody derived antigen recognition domain do

A

recognizes cancer cells

75
Q

how do they get the antibodies for CAR

A

from the same patient

76
Q

where do “off the shelf” allogenic CAR T cells come from

A

healthy donors then recombinant DNA

77
Q

what is the role of co inhibitory immune checkpoints

A

prevent aberrant or chronic activation of the immune system

78
Q

how do cancer cells use the co inhibitory immune checkpoints

A
  • to damped anti-tumor T cell responses

- promote tumor immune escape

79
Q

what do checkpoint blockage therapies do to the immune system (which phases)

A

reactivate induction and effector phases of anti-tumor T cell responses

80
Q

what happens with CTLA4 checkpoint blockade

A

supports the induction phase of anti-tumor T cell responses

81
Q

what happens with PD1 checkpoint blockade

A

maintains the effector phase of anti tumor T cell responses

82
Q

what is ipilimumab

A

fully human mAb against CTLA4

83
Q

what is the mechanism of ipilimumab

A

blocks interaction of CTLA4 with CD80 86 during antigen presentation in lymph nodes

84
Q

what is the result of ipilimumab

A

promotes T cell production and disinhibits T cell response expansion

85
Q

what % of human cancer express PD-L1

A

20-50%

86
Q

what can upregulate PDL1 expression on tumor cells

A

constitutive oncogenic signalling

87
Q

what are 2 drugs that treat the PD cycle

A

Nivolumab and Atezolizumab

88
Q

what is Atezolizumab

A

Fully humanized mAb against PDL-1

89
Q

what is Nivolumab

A

Fully humanized Ab against PD-1

90
Q

what are 2 things that Atezolizumab cause

A
  • reduce immunosuppressive signals in tumor microenvironment

- increase T cell mediates immunity against tumor

PMCOL 344 (27 decks)

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