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GBA Immunology > Week 14 - Cancer and Gestational Immunology > Flashcards

Week 14 - Cancer and Gestational Immunology Flashcards

1
Q

What are the two edges of Tumor Homeostasis scale?

A

Tumor suppressor gene effects Vs. (Proto)oncogene effects

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2
Q

Phases of Tumors:

A 
Tumorigenesis
Elimination 
Equilibrium 
Escape
(3Es)
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3
Q

_____ _______ is the first step of tumorigenesis!

A

Chronic inflammation is the first step of tumorigenesis!

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4
Q

macrophages, mast cells, eosinophils, fibroblasts, platelets and endothelial cells are shared cells in:

A

Tumorigenesis

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5
Q

CXCL1,2,3,5,8, VEGF, bFGF, TGFb, PDGF are shared Cytokines in:

A

Tumorigenesis

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6
Q

MMP-2, MMP-9 and uPA are all Shared matrix degrading

mechanisms for:

A

Tumorigenesis

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7
Q

Elimination - Signs of cellular stress:

A

ULBP1,2,3 and MICA

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8
Q

Elimination - signs of avoidance of adaptive immunity:

A

Reduction of MHC protein expression / lacking KIR (missing self recognition).

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9
Q

Elimination -Cells involved:

A

γ𝛿 T-cells and Natural Killer cells

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10
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
What are they? (Not examples - Meaning)

A

These are associated with tissue injury and cell death.

Could signal of an emerging tumor.

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11
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: Extracellular DNA and RNA

A

DC activation and maturation

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12
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: Urea crystals

A

DC maturation

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13
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: HMGB1 (chromatin protein)

A

DC Ag uptake/presentation

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14
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: HSP70, HSP90

A

DC cross-presentation

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15
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: Calreticulin

A

Phagocytosis by DCs

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16
Q

Elimination- Danger signals recognized by dendritic cells (DCs):
Name the DC response for: Phosphatidylserine, integrin

A

recognition by DCs (“EAT ME SIGN”)

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17
Q

Elimination- γ𝛿 T-cells and Natural Killer cells Mechanisms of Induction of Apoptosis: (At least 5)

A
  • Perforin/granzyme
  • TNF
  • TRAIL-TRAILR1/2 contact
  • IFNα/β
  • IFNγ (also enhancement of the Tc/Th1 response)
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18
Q

Elimination- M1 cells Mechanisms of Induction of Apoptosis:

A
  • Reactive oxygen radicals (ROI) -> tissue injury

- TNF

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19
Q

What are M1 cells?

A

Th1-polarized, tumor associated macrophage

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20
Q

Elimination – recognition of tumors by the adaptive
immune a system:
Products of Mutated Oncogenes and Tumor Suppressor Genes Examples

A

RAS

P53

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21
Q

Elimination – recognition of tumors by the adaptive

immune a system: Overexpressed or Aberrantly Expressed Cellular Proteins Example (Extra Knowledge)

A

MAGEA1

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22
Q

Elimination – recognition of tumors by the adaptive

immune a system: Oncogenic Virus antigens Examples

A

EBV

HPV

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23
Q

Elimination – recognition of tumors by the adaptive

immune a system: Oncofetal antigens Examples (Extra Knowledge)

A

CEA

AFP

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24
Q

Elimination – recognition of tumors by the adaptive

immune a system: Altered Cell Surface Glycolipids and Glycoproteins Example (Extra Knowledge)

A

MUC1

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25
Q

CD_+ T-cells are the main effectors of anti-tumor immunity!

A

CD8+ T-cells are the main effectors of anti-tumor immunity!

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26
Q

Tumor antigens released by the tumors can be taken up by APCs, but exogenous antigens are in the
groove of MHC II. What is the Problem with this fact?

A

Naive CD8+ T cells recognize antigens presented with MHC I in the lymph nodes. Therefore CD8+ T cells do not recognize them!

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27
Q

What is Cross-presentation? (Solving the Problem of the Other Question)

A

Under special conditions APCs may present exogenous antigens with MHC-I to CD8+ T cells

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28
Q

Requirements for Cross-presentation:

DC licensing from CD4+ Th1 cells by -

A

CD40 Interaction of CD4+ T cell

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29
Q

Requirements for Cross-presentation:

Danger signal for DCs -

A

TLR7 stimulation (RNA) - General Example

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30
Q

Requirements for Cross-presentation:

Support for CD8+ T cell survival -

A

IL-2 ↑

PDL1 ↓ (Programmed Death Ligand 1)

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31
Q

Cancers in which increased T-cell infiltration

associates with ____ prognosis.

A

Cancers in which increased T-cell infiltration

associates with better prognosis.

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32
Q

The Immunoscore is a method to estimate the ______ of cancer patients, based on the _____ cells that infiltrate cancer and surround it. It has been internationally validated in _______ cancer.

A

The Immunoscore is a method to estimate the prognosis of cancer patients, based on the immune cells that infiltrate cancer and surround it. It has been internationally validated in colorectal cancer.

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33
Q

2 methods of Antibody-mediated lysis of Tumors:

A

1) Complement-activation

2) ADCC

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34
Q

Equilibrium: Intact, organized T cell responses present

even in _______ colorectal cancer

A

Equilibrium: Intact, organized T cell responses present

even in advanced colorectal cancer

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35
Q

Equilibrium: T cell/ T Cytotox gene activity ______ correlates with chance for a relapse.

A

Equilibrium: T cell/ T Cytotox gene activity inversely correlates with chance for a relapse.

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36
Q

Escape - corruption of dendritic cells (DC) and antigen presentation: Inefficient uptake of tumor antigens - How is this Achieved?

A

Inhibition of DC endocytosis

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37
Q

Escape - corruption of dendritic cells (DC) and antigen presentation: Number of mature DC in the tumor and
draining lymph nodes↓ - How is this Achieved?

A

Inhibition of DC immigration / emigration

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38
Q

Escape - corruption of dendritic cells (DC) and antigen presentation: Antigen presentation↓ - How is this Achieved?

A

Inhibition of MHC I/II expression in DC

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39
Q

Escape - corruption of dendritic cells (DC) and antigen presentation: Tolerance against presented tumor antigens - How is this Achieved?

A

Down-regulation of DC costimulatory

molecules (CD80/86)

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40
Q

Escape - corruption of dendritic cells (DC) and antigen presentation: Trp, Arg deprivation (key metabolites for T
cells) in T cells, CD8+ T anergy and apoptosis↓, Treg
differentiation ↓, bystander DC also become tolerized ↓- How is this Achieved?

A

Induction of IDO (indoleamine 2,3-

dioxygenase) and Arginase expression

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41
Q

Escape – various other mechanisms:

Tumor cells avoid CD8+ T cell recognition - How is this Achieved?

A

Cessation of MHC I expression

42
Q

Escape – various other mechanisms:

Antigen masking - How is this Achieved?

A

Immunogenic cell surface Ags disappear

from cancer cells via endocytosis

43
Q

Escape – various other mechanisms:

Antigen shedding - How is this Achieved?

A

Alternative splicing or proteolytic degradation of the antigen allows production of a soluble form and shedding.

44
Q 
Escape – various other mechanisms:
Barrier formation (immune privilege) - How is this Achieved?
A

Hard to penetrate ECM-shell or Factors are secreted from the Tumor to Produce a Shell

45
Q

Escape – various other mechanisms:

Tumor burden - How is this Achieved?

A

Exhaustive effect on the host, IS

46
Q

CSC-driven tumorigenesis (new model): Tumors are ___________ but only a ___ ________ of all tumor cells, the cancer stem cells proliferate, self-renew and form new lesions effectively.

A

CSC-driven tumorigenesis (new model): Tumors are heterogeneous but only a tiny fraction of all tumor cells, the cancer stem cells proliferate, self-renew and form new lesions effectively.

47
Q

Cancer stem cells, like many other stem cells are, compared to the majority of tumor cells -they are: (2)

A

A) less immunogenic

B) more resistant to immune-mediated lysis

48
Q

M1 macrophages (Th1-polarized), NK, NKT, γ𝛿 T, CD8+ T cells, CD4+T cells, mDC-k (mature DCs) - are all examples for cells that Promote Tumor ______ and Part of the _____ Inflammation process.

A

M1 macrophages (Th1-polarized), NK, NKT, γ𝛿 T, CD8+ T cells, CD4+T cells, mDC-k (mature DCs). These are all examples for cells that Promote Tumor Rejection and Part of the Acute Inflammation process.

49
Q

M2 macrophages (Th2-polarized), MDSC-k (Myeloid-Derived Suppressor Cell:CD11b+ /GR1+ myeloid cells) Mast cells, D25+ Foxp3+ Treg, iDC-k (immature DCs), Immune complex deposition - are all examples for cells that Promote Tumor ______ and Part of the _____ Inflammation process.

A

M2 macrophages (Th2-polarized), MDSC-k (Myeloid-Derived Suppressor Cell:CD11b+ /GR1+ myeloid cells) Mast cells, CD8+ T cells, CD4+ T cells, D25+, Foxp3+. Treg, iDC-k (immature DCs), Immune complex deposition - are all examples for cells that Promote Tumor Escape and Part of the Chronic/Abnormal Inflammation process.

50
Q

What are the cytokines Tumor secrete in order to promote escape?

A

immunosuppressive cytokines :IDO, IL-10, TGFβ and VEGF

51
Q

Escape: Local Effects -T cell anergy with recruitment of abnormal inflammatory cells ___: Ag presentation without _________.

A

Escape -T cell anergy with recruitment of abnormal inflammatory cells iDC (immature DC): Ag presentation without costimulation.

52
Q

Escape: Local Effects - NOS

A

NO Synthesis and Arginase Production

53
Q

Escape: Local Effects - reduction of the T cell lifespan by the tumor:

A

TRAIL or PDL1 expression

FasL are a Hypothesis

54
Q

Escape: Systemic effects -

interference with _ cell signaling

A

Escape: Systemic effects -

interference with T cell signaling

55
Q

Escape: Systemic effects -

reduced ____ ____ chain expression

A

Escape: Systemic effects -

reduced CD3+ zeta chain expression

56
Q

Escape: Systemic effects -

inhibition of ____ activation

A

Escape: Systemic effects -

inhibition of NF-kB activation

57
Q

Escape: Systemic effects -

interference with the ____ signaling

A

Escape: Systemic effects -

interference with the STAT signaling

58
Q

Escape – Immunoediting - Definition

A

Unsuccessful attempts to eliminate cancer over a long time, sooner or later inevitably select out tumor cells that are resistant to most antitumor immune mechanisms (the tumor is ”edited” by the IS).

59
Q

Rituximab, Ibritumomab, Tositumomab, Alemtuzumab, Gemtuzumab…etc - These are:

A

FDA-approved immunotherapies - Monoclonal antibodies

60
Q

BCG, Imiquimod - These are:

A

FDA-approved immunotherapies - Adjuvants

61
Q

What are the Cytokines given as a FDA-approved immunotherapies ?

A

IFNa, IL-2, TNFa

62
Q

What are examples of Supportive therapies given as a FDA-approved immunotherapies ?

A

G(M)-CSF (Myelosuppressive)

Leucovorin (MTX Rescue)

63
Q

FDA-approved immunotherapies - Prophylaxis for:
HPV vaccine and HBV vaccine :
Antibiotics:
NSAID (FAP, ulc. colitis):

A

FDA-approved immunotherapies - Prophylaxis for:
HPV vaccine and HBV vaccine : Oncogenic Viruses
Antibiotics: Removal of Oncogenic Bacteria (H.Pylori)
NSAID (FAP, ulc. colitis): Inhibition of Chronic Inflam.

64
Q

Bone marrow transplantation - 2 options

A

Allogeneic and DLI

65
Q

Blockade of tumor receptors promoting growth Induction of apoptosis via receptors,
Complement mediated lysis of tumor cells, ADCC against tumor cells, Carrying a prodrug, a toxin, or a radioactive isotope to tumor cells. These are all examples for _________ _____-based immunotherapies.

A

Blockade of tumor receptors promoting growth Induction of apoptosis via receptors,
Complement mediated lysis of tumor cells, ADCC against tumor cells, Carrying a prodrug, a toxin, or a radioactive isotope to tumor cells. These are all examples for Monoclonal antibody-based immunotherapies.

66
Q

Example: Treatment of Basal cell carcinoma with Imiquimod /Aldara (TLR7 agonist) - This is an example of ______-based tumor immunotherapies. This causes a conversion of the Chronic ____ controlled Inflammation to an Acute one.

A

Example: Treatment of Basal cell carcinoma with Imiquimod /Aldara (TLR7 agonist) - This is an example of Adjuvant-based tumor immunotherapies. This causes a conversion of the Chronic Tumor controlled Inflammation to an Acute one.

67
Q

Tumor antigen-based immunotherapies: active specific immunization - could be achieved by a ____ of allogeneic tumor cells mixed with PAMPs

A

Tumor antigen-based immunotherapies: active specific immunization - could be achieved by a lysate of allogeneic tumor cells mixed with PAMPs

68
Q

Tumor antigen-based immunotherapies: active specific immunization - ______ tumor antigens
mixed with PAMPs

A

Tumor antigen-based immunotherapies: active specific immunization - conserved tumor antigens
mixed with PAMPs

69
Q

Tumor antigen-based immunotherapies: active specific immunization - tumor cells that were genetically modified to express _____________ cytokines (add and Example).

A

Tumor antigen-based immunotherapies: active specific immunization - tumor cells that were genetically modified to express immunostimulatory cytokines (e.g. GM-CSF to support DC maturation).

70
Q

Tumor antigen-based immunotherapies - Stopping spontaneous or tumor-induced T-cell suppression:
CTLA-4 blockade (In T Cells), How is it helpful?

A

Eliminates Tumor Inhibition of DC-T cells co-stimulation and Tumor recognition

71
Q

What causes expression of PDL1 on Tumor cells? (2)

A

1) Constitutive Oncogenic Signaling

2) T-cell Induction

72
Q

Tumor antigen-based immunotherapies - Stopping spontaneous or tumor-induced T-cell suppression:
- PD-1 blockade (In T Cells), How is it helpful?

A

Eliminates Tumor Negative regulation CD8+T cells.

73
Q

Tumor antigen-based immunotherapies - Stopping spontaneous or tumor-induced T-cell suppression:
- PDL1 blockade (In Tumors), How is it helpful?

A

Eliminates Tumor Negative regulation CD8+T cells.

74
Q

In contrast to targeted therapies, _____ _______ ______ induces long term responses, but only in a fraction of all patients.

A

In contrast to targeted therapies, Immune checkpoint blockade induces long term responses, but only in a fraction of all patients.

75
Q

Cancers with ____ rate of genomic ______ are the

most responsive to ICB (e.g. _______)

A

Cancers with high rate of genomic mutations are the

most responsive to ICB (e.g. melanoma)

76
Q

Current antitumor immunotherapies - virotherapies:

Oncovirus is an ________ virus that invades both Healthy cells and _____ cells.

A

Current antitumor immunotherapies - virotherapies:

Oncovirus is an attenuated virus that invades both Healthy cells and Tumor cells.

77
Q

Current antitumor immunotherapies - virotherapies:
Oncovirus ______ in the tumor cell and causes eventual _____ releasing: TSAs and _______ and causing acute inflammation and _______ of tumor.

A

Current antitumor immunotherapies - virotherapies:
Oncovirus replicates in the tumor cell and causes eventual lysis releasing: TSAs and GM-CSF and causing acute inflammation and rejection of tumor.

78
Q

Current antitumor immunotherapies - virotherapies:

Oncovirus is an ________ virus that is doesn’t ______ in healthy cells.

A

Current antitumor immunotherapies - virotherapies:

Oncovirus is an attenuated virus that is doesn’t replicate in healthy cells.

79
Q

Current antitumor immunotherapies - Adoptive cell transfer (ACT): Tumor fragments cultured in ____, Induction of tumor infiltrating ____ T cell (TIL) proliferation with ___ and finally Re-introduction of tumor-specific ____ T cells that have been massively cultured.

A

Current antitumor immunotherapies - Adoptive cell transfer (ACT): Tumor fragments cultured in vitro, Induction of tumor infiltrating CD8+ T cell (TIL) proliferation with IL-2 and finally Re-introduction of tumor-specific CD8+ T cells that have been massively cultured.

80
Q

CAR therapy - What is the meaning of the name?

A

T cells receive tumor-specific CHIMERIC BCR-ANTIGEN RECEPTOR (CAR therapy) via gene editing.

81
Q

CAR therapy example - T cells with anti-CD19

BCR to treat CD19+ B-___.

A

CAR therapy example - T cells with anti-CD19

BCR to treat CD19+ B-ALL.

82
Q

CAR therapy 1st generation: scFv anti-CD19- BCR fusioned with ____ to provide TCR-like signals by the BCR.

A

CAR therapy 1st generation: scFv anti-CD19- BCR fusioned with CD3ε to provide TCR-like signals by the BCR.

83
Q

CAR therapy 2nd generation: scFv anti-CD19- BCR fusioned with CD3e and ____/______ domains to provide co-stimulation too.

A

CAR therapy 2nd generation: scFv anti-CD19- BCR fusioned with CD3e and CD28/4-1BBL domains to provide co-stimulation too.

84
Q

CAR therapy 3rd generation: scFv anti-CD19-BCR fusioned with CD3e and ____ independent costimulatory _______.

A

CAR therapy 3rd generation: scFv anti-CD19-BCR fusioned with CD3e and multiple independent costimulatory domains.

85
Q

scFv: What is it ? What does it contain?

CAR therapy

A

Single-chain variable fragment. Containing genetically engineered VH and VL subdomains for BCR function in modified CAR T cells.

86
Q

CAR therapy can be combined with:

A

Immune checkpoint blockade.

87
Q

Elimination Early classification: ____-______ ______ (TSA), which are present exclusively on tumor cells (rare) and _____-________ _______ (TAA), which are present both on tumor and normal normal cells.

A

Elimination Early classification: Tumor-Specific Antigens (TSA), which are present exclusively on tumor cells (rare) and Tumor-Associated Antigens (TAA), which are present both on tumor and normal normal cells.

88
Q

The fetus is a ____-allograft.

A

The fetus is a hemi-allograft.

89
Q

The fetus as hemiallograft - Name the Immunological Viewpoint Matching the Physiological one : Insemination

A

Transplantation

90
Q

The fetus as hemiallograft - Name the Immunological Viewpoint Matching the Physiological one :Pregnancy

A

Tolerance

91
Q

The fetus as hemiallograft - Name the Immunological Viewpoint Matching the Physiological one : Abortus

A

Acute rejection

92
Q

The fetus as hemiallograft - Name the Immunological Viewpoint Matching the Physiological one :Birth

A

Timely rejection

93
Q

Recognition of fetal antigens by the mother - Antibodies against paternal antigens in __% of primiparae, in __-__% in multiparae .

A

Recognition of fetal antigens by the mother - Antibodies against paternal antigens in 20% of primiparae, in 40-60 % in multiparae.

94
Q

Presentation of fetal antigens:
• No ______ on trophoblast cells
• Monomorphic _____-like molecules:
_____, _____: Inhibition of CD8+ T cells and NK cells

A

Presentation of fetal antigens:
• No MHC-II on trophoblast cells
• Monomorphic MHC I-like molecules:
HLA-G, HLA-E: Inhibition of CD8+ T cells and NK cells

95
Q

Immunosuppression in pregnancy: associated cells

A

γ𝛿 T-cells and T-Reg cells

96
Q

Which Cytokines are used by γ𝛿 T-cells and T-Reg cells in Immunosuppression in pregnancy?

A

TGF-β, Th2 cytokines

97
Q

Which Endocrine factors released by fetus are contributing to Immunosuppression in pregnancy?

A

Endocrine - Fetal:

• α-1-fetoprotein

98
Q

Which Endocrine factors released by mother are contributing to Immunosuppression in pregnancy?

A

Endocrine - Maternal:
• Progesterone, estrogen
• Placental (chorion)
• hCG

99
Q

What is PIBF?

A

Progesterone induced blocking factor

100
Q

Effects of PIBF

  1. __ cells are inhibited
  2. Th-2 cytokine _____
  3. anti-_____ effects
  4. inhibits ________ metabolism
  5. Asymmetric antibodies _____
A

Effects of PIBF

  1. NK cells are inhibited
  2. Th-2 cytokine excess
  3. anti-abortive effects
  4. inhibits arachidonic metabolism
  5. Asymmetric antibodies elevated

GBA Immunology (15 decks)

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