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I&I WC2 > Tumor Immunology II > Flashcards

Tumor Immunology II Flashcards

Eerst lecture Mandy, dan college II Sonja

1
Q

What are the seven steps of the tumor-immunity cycle?

A
  1. Tumor ag release
  2. Ag-uptake by DC
  3. T-cell priming
  4. T-cell trafficking
  5. T-cell infiltration
  6. Ag-recognition
  7. Tumor killing
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2
Q

Why can T cells traffic into the tumor?

A

Because they are primed with tumor antigens

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3
Q

Name three examples how tumors can inhibit T cell killing

A
  1. Checkpoints presented in tumor tissues
  2. Thick stromal layer
  3. Inhibition of the number of DCs that present antigen in the LN
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4
Q

Name two ways by which antigen presentation by DCs can be enhanced to boost the anti-tumor immune response?

A
  1. In vivo targeting
  2. Adoptive transfer of ex vivo loaded and activated DCs
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5
Q

At which step of the tumor immunity cycle does DC-therapy interfere?

A

T cell priming in the LN

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6
Q

Why can DC-therapy lead to a more effective anti-tumor immunity cycle?

A

Because they are primed

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7
Q

What are ways to manipulate DCs in- or ex vivo? Administration of? (3)

A
  1. DC-activating factors
  2. DC-mobilizing agents
  3. Antigens/adjuvant
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8
Q

Why can we not make a vaccine based on the DC subsets that we isolate from the peripheral blood?

A

Only few DC subsets are present in the peripheral blood

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9
Q

Which cells are used for DC vaccines?

A

Monocyte-derived DCs

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10
Q

Which compound can be used to mature DCs?

A

Growth factors; GM-CSF

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11
Q

How long does it take to create one DC vaccine?

A

10 days

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12
Q

How are DCs loaded with antigens?

A

Antigen pulsing

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13
Q

What is meant with an “autologous setting” in DC vaccination?

A

You use tumor material from the mice/patient itself

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14
Q

What is meant with an “allogeneic setting” in DC vaccination?

A

Material that is used to load DCs is not genetically identical to the material that is present within the patient

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15
Q

Which allogeneic setting approach can be used for DC vaccine formation?

A

Tumor cell lines of multiple patients -> mix them

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16
Q

How can we further enhance DC-therapy efficacy? (2)

A
  1. Targeting TAM phenotype
  2. Combination with checkpoint blockade
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17
Q

What are TAMs?

A

Tumor-associated macrophages -> present within tumor tissue

18
Q

Which phenotype are TAMs associated with?

A

Suppressive phenotype -> inhibit anti-tumor response

19
Q

What are the three main mechanisms by which TAMs can inhibit the immune system?

A
  1. Direct suppression T cells
  2. Induce Tregs
  3. Inhibit DC maturation
20
Q

What is the goal of using antibodies to block the PD1/PD1L axis?

A

Better activation and function of T cells

21
Q

Why is the dogma that the PD1/PD1L axis is only important in the tumor site not really valid anymore?

A

Axis also present within the TDLN -> can hamper T cell priming by DCs

22
Q

Which two in vivo DC targeting approaches did Sonja zoom in on in her second lecture?

A
  1. Synthetic long peptides
  2. mRNA vaccines
23
Q

Why do you often need a proliferation step for immune monitoring of vaccine responses?

A

Often T cells in the blood are of low frequency

24
Q

What are the different assay you can use for immune monitoring of vaccine responses? (4)

A
  1. IFNy ELISA
  2. IFNy ELISPOT
  3. Flow cytometry
  4. Changes in TCR clonality/diversity
25
Q

Which assay can be used directly ex vivo for immune monitoring of vaccine responses? Why?

A

ELISPOT -> sensitive

26
Q

What is indicative of a nice and potent response upon vaccination?

A

Clear result directly ex vivo using ELISPOT

27
Q

How can you determine which cells make the cytokine using ELISPOT?

A

Sort them in advance

28
Q

Which subset of patients benefits from a vaccine that broadens the T cell repertoire?

A

Some patients have low clonality to begin with

29
Q

What is the main advantage of using SLPs as vaccination strategy?

A

Shelf life of several years

30
Q

What is Sonja’s opinion on the usage of SLP vaccines? Which purpose seems ideal?

A

Generic vaccines

31
Q

What is Sonja’s opinion on the usage of mRNA vaccines? Which purpose seems ideal?

A

Personalized vaccines

32
Q

What is the main aim of the development of therapeutic vaccines for chronic HBV infection?

A

Getting rid of all antigen and DNA in the blood

33
Q

What can be said about the T cell response in chronic HBV infection?

A

Very low T cell responses (mostly exhausted)

34
Q

What causes the very low (exhausted) T cell responses in HBV infection? (2)

A
  1. Antigen overexposure
  2. Lack of effective priming
35
Q

How does an UV-based in vitro HLA binding assay work? (6)

A
  1. Loading HLA complex with UV cleavable peptide
  2. Expose to UV
  3. Peptide broken down
  4. Peptide falls out of complex -> complex falls apart
  5. Expose complex to to peptide of interest
  6. If the peptide can bind, it rescues the falling apart -> takes place of UV cleaved peptide
36
Q

Why do we not have to predict epitopes for HLA-II?

A

HLA-II is present at such an ambiguous level -> we get them for free

37
Q

Which areas of a viral genome can you best use for epitope mapping to develop a SLP-based vaccine (HBV)?

A

Areas on the viral genome that the virus needs to propagate -> will be conserved

38
Q

Why are chronic HBV patients responding better to SLP-vaccination than resolvers?

A

Resolvers could have cleared disease a long time ago -> memory population very small

39
Q

SLP design is based on..? (5)

A
  1. Epitope distribution
  2. Conservation
  3. HLA coverage
  4. Functional domains
  5. Synthesizeability
40
Q

Hepatitis: immunopeptidomics for the selection of best SLPs can be done on? (3)

A
  1. Antigen loaded DC
  2. Diseased hepatocytes
  3. HBV expressing HCC cell-line
41
Q

What is the basic SLP discovery pipeline?

A
  1. Identify target proteins
  2. Identify conserved regions
  3. Predict whether these conserved regions contain epitopes that can be presented by DCs
  4. Design SLP

I&I WC2 (22 decks)

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