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Immunolgy > Cancer Immunology > Flashcards

Cancer Immunology Flashcards

1
Q

What is central tolerance and peripheral tolerance?

A

Self-reactive T cells are eliminated during development (central tolerance)

T cells are inactivated in the periphery (peripheral tolerance)

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2
Q

Give 3 examples of antigens derived from self-molecules that escape T cell tolerance (3 points)

A
  • Cancer/testis antigens (CTag)
  • Differentiation antigens
  • Oncofoetal antigens
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3
Q

What are Neoantigens? (1 point)

A

Antigens derived from genes mutated in the cancer

  • Any gene with a coding sequence changed from the wild-type has the ability to be a neoantigen
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4
Q

Where are cTag antigens found and what do they play a role in? (2 points)

A

Cancer/testis antigens (CTag) - found in developing testes - play a role in malignancy - MAGE molecules

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5
Q

What are differentiation antigens, and where are they found? (2 points)

A

Differentiation antigens - expressed at low levels in normal development - but greatly increased in tumour cells - e.g., tyrosinase in melanoma

  • Are antigens derived from self-molecules that escape T cell tolerance mechanisms
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6
Q

Where are oncofoetal antigens found? And what are they?

2 points

A

Oncofoetal antigens - expressed during embryonic development before T cell development - e.g., CA125 - Carcinoembryonic antigen (CEA)

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7
Q

Name 2 other cancer-specific alterations in proteins

2 points

A
  • Changes in post-translational modifications (MUC family molecules)
  • Aberrant splicing products (generating new coding sequence)
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8
Q

Name the three types of tumour associated antigens

3 points

A
  1. Antigens derived from self-molecules that escape T cell tolerance mechanisms
  2. Neoantigens
  3. Other cancer-specific alterations in proteins
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9
Q

What is NY-ESO-1?

A
  • New York oesophageal squamous cell carcinoma

- Generates both antibody and T cell responses

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10
Q

What are the 3 E’s?

A

Elimination, equilibrium, escape

  • Thought to be how the immune system sculpts cancer
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11
Q

Name 4 viruses that have evolved mechanisms to prevent MHC 1 molecules from reaching the surface
(4 points)

A
  • Herpesviruses
  • HPV 16 and 18
  • Adenoviruses
  • HIV
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12
Q

What two receptors do NK cells have?

2 points

A
  • Killer inhibitory receptors - binds to MHC1 and turns off NK cell
  • Activating receptor - e.g., NKG2D - kills cell and releases pro-inflammatory cytokines
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13
Q

How do NK cells target tumours? (2 points)

A
  • Cell division of cancer cells drives cell cycle genes and presents surface ligands e.g., NKG2D
  • Accumulation of NKG2D overcomes the MHC1 signal and so the NK cell is activated and targets the cancer cells
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14
Q

How do tumours evade immunity? (9 points)

A
  • Loss of antigen
  • Loss of MHC1
  • Loss of activating ligands - e.g., NKG2D
  • Recruitment of suppressive immune cells - e.g., Treg, M2-like macrophage and Myeloid Derived suppressor cells (MDSC)
  • Secretion of immunosuppressive cytokines - IL-10, TGF-beta
  • Metabolic competition with tumour cells
  • Secretion of inhibitory metabolites
  • Apoptosis of immune cells
  • Initiation of immune checkpoints
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15
Q

What are immune checkpoints? (2 points)

A
  • Naturally occurring feedback inhibitors of an immune response - e.g., PD-1
  • Checkpoint molecules inhibit the T-cell and self limit the immune response - prevents killing of healthy cells
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16
Q

What does IFN-gamma/oncogene activity do to tumour cells? (2 points)

A
  • IFN-gamma induces PD-L1- (ligand for PD-1) on tumour cells
  • This inhibits T cells from PD-1-PDL-1 interaction - even if the correct antigen and T-cell receptor is present
17
Q

What does TGF-beta do for tumours? (1 point)

A
  • Counteracts immune cells brought to the tumour after T cell activation.
18
Q

Three examples of immunotherapy of cancer (3 points)

A
  • Antibody targeting of tumour cells
  • T cell targeting of tumour cells
  • Inhibiting immune checkpoints with antibodies
19
Q

What is rituximab (anti-CD20) and how does it work?

3 points

A
  • Treatment for lymphoma - also used for arthritis
  • Is a chimeric therapeutic antibody - Fc receptors on NK cells recognise IgG and induce Antibody dependent cellular cytotoxicity (ADCC)
  • Triggers complement pathway - initiates complement mediated cytotoxicity (CMC) - kills tumour
20
Q

What is CD20? (2 points)

A
  • A marker on B-cells - shows normal healthy B-cells

- Cross linking of CD20 induces apoptosis and sensities to chemotherapy

21
Q

Brief explanation of T cell retargeting (3 points)

A
  • Uses chimaeric antigen receptor (CAR) T cells
  • Replace T cell receptor with different antigen receptor - and activated using antibodies
  • T cells are injected back into patient and now express new receptor and mediate anti tumour activity
22
Q

What are the problems with CAR T cells? (4 points)

A
  • Logistics - need to be specifically made for each patient
  • Very expensive
  • Toxicity - T cells are very powerful and CAR T cells have bypassed the normal safeguards for self-reactivity
  • Adverse effects are common - and can be life threatening
23
Q

How does the immune checkpoint blockade work?

4 points

A
  • Blocks the interaction between PD-1 and PDL-1
  • Can use antibody against either PD-1 or PDL-1
  • Used for other immune checkpoints also
  • Wakes T cells up and allows them to continue to kills tumour cells - only activation signal

Immunolgy (8 decks)

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