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Immunolgy > Immunotherapy > Flashcards

Immunotherapy Flashcards

1
Q

Name 5 novel therapeutic strategies of immunotherapy

A
  • Biologics
  • Adjuvants
  • Allergy Immunisation
  • Helminithic therapy
  • Cancer therapy
  • T-cell engineering
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2
Q

Name 4 conventional immunosuppressive drugs

A
  • Corticosteroids
  • Cytotoxic drugs
  • Cyclosporin A
  • Rapmycin
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3
Q

How do corticosteroids work?

A

Inhibit inflammation

  • Inhibit transcription of inflammatory genes
  • Promote transcription of anti-inflammatory genes
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4
Q

How do Cytotoxic drugs work?

A

Interfere with DNA synthesis

  • Non specific - e.g., azathioprine, cyclophosphamide, mycophenolate
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5
Q

How does Cyclosporin A work?

A

suppresses IL-2 - inhibits T-cell proliferation

  • via NFAT
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6
Q

How does rapymycin work?

A

Inhibits mTOR pathway - inhibits cell proliferation, translation and auto-Nagy

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7
Q

Definition of Immunotherapy

A

Treating disease via immune modulation - activation, suppression or skewing

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8
Q

4 methods of immunotherapy

A
  • Soluble mediators - cytokines, cytokine antagonists, adjuvants
  • Antibody therapy - receptor/ligand blocking
  • Cell based - DC vaccination/ genetic engineering of T-cells
  • Skewing/suppression
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9
Q

4 examples of cytokines in immunotherapy

A
  • GM-CSF/G-CF (growth factors) - treats neutropenia in cancer patients - increases WBCs
  • PEGylated interferon alpha - treats hepatitis B/C (viral infection)
  • Bone marrow donors - injection - increases WBCs
  • Interferon gammar - treats CGD patients - activates macrophages/neutrophils
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10
Q

3 examples of cytokine antagonists

A
  • Anakinra - soluble IL-1 receptor antagonist - targets auto inflammatory diseases
  • Rilonacept - IL-1-Fc fusion protein
  • Etanercept - recombinant TNF-alpha receptor-fusion protein
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11
Q

3 examples of adjuvants

A
  • CpG (ligand) - imiquimod - cancer/warts
  • Beta glucans - yeast cell walls
  • Hypomethylated DNA - activate toll-like receptors - useful for viral/type-1 response
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12
Q

what is CTLA-4 and what do CTLA-4 inhibitors do?

A
  • CTLA-4/CD152 protein receptor - is an immune checkpoint and downregulates immune responses
  • Checkpoint inhibitors - like anticancer drugs block CTLA-4 - which inhibits T-cell costimulation
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13
Q

3 examples of the therapeutics of monoclonal antibodies

A
  • Anti-TNF-alpha - major pro inflammatory cytokine (infliximab)
  • B-cell leukaemia anti-CD20 - (Rituximab)
  • Breast cancer - anti-HER2/neu receptor - (Herceptin/trastuzamab)
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14
Q

Modes of action of monoclonal antibodies

A
  • Ligand/receptor blocking
  • Induction of apoptosis
  • Complement mediated killing
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15
Q

Problems with monoclonal antibodies

A
  • Expensive
  • Hard to copy
  • Repeat doses are often immunogenic - neutralising anti-antibody antibodies
  • Can humanise antibody - but keeps loops as mice/rat - which are less immunogenic
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16
Q

What is the role of adjuvants?

A
  • Enhance immune response
  • Upregulate costimulatory molecules - increase migration and presentation to DCs - increases longevity of antigen
  • pore proteins are not immunogenic - so you need to add adjuvants
  • magnitude and type of response can be manipulated via coupling and type of adjuvant used
17
Q

What is squalene used for ?

A
  • Is a lipid - added to adjuvants as soluble adjuvants can be cleared by circulation easily
18
Q

How are allergies caused? (1 point)

A
  • Excessive Th2 immunity

- Th2/IgE mediated response activate mast cell degranulation - and cause inflammation and tissue damage

19
Q

How can immunotherapies prevent allergies?

6 points

A
  • By suppressing/skewing the Th2 response to a Th1 response
  • By immunising APC or DC
  • Enhancing Th1 = Switches off Th2
  • Stops generation of IgE
  • Can use mutated allergens - with agonists - leads to IgG response e.g., CpG/TLR4
  • Higher dosage of allergen - T reg cells can switch off Th2 response
20
Q

Why is dangerous too inject allergens? (1 point)

What can you do to stop this? (1 point)

A
  • Can cause anaphylactic shock

- Can inject anti-IgE therapy

21
Q

Examples of diseases caused by excessive Th1/Th17 immunity? (4 points)

A
  • Inflammatory bowel disease
  • Type 1 diabetes
  • Multiple sclerosis
  • Rheumatoid arthritis
22
Q

What are helminths and what are they used for?

2 points

A
  • are parasitic worms
  • Can be used to skew immune system from Th1 to Th2 - so Th2 will regulate Th1
  • uses dendritic cells
23
Q

How do you use tolergenic dendritic cell therapy to suppress the immune response and what can it prevent? (3 points)

A
  • Remove DCs and grow in growth factor - to form tolergenic DCs.
  • Inject into human - helps switch off T cells directly, generate T reg cells (to switch off T cells) or cause T cells to undergo apoptosis
  • prevent allergy or inflammatory type 1/2 disease
24
Q

What is transplantation and name 2 methods?

A
  • Prevention of transplant rejection

- Can use long term immunosuppressives or short term

25
Q

What are used as long term immunosuppressives and why are they not good?

A
  • Corticosteroids

- Can mean patient is immunocompromised for a long time

26
Q

How do short term immunosuppressives work?

And name 3 examples? ( 3 points)

A
  • Induce T cell unresponsiveness - ‘reset’ tolerogenic mechanisms
  • Campath-1 monoclonal antibody
  • Basiliximab - prevents T cell activation (anti-IL-2 receptor)
  • Non-FcR binding anti CD3 monoclonals - anti-alpha-Beta- TcR monoclonals
27
Q

How do tumours grow? (2 points)

A
  • Create anti-inflammatory environment - switch off immune cells
  • use inhibitory receptors that switch them off
28
Q

Name 4 ways to enhance immune response against cancerous tumours? (4 points)

A
  • Checkpoint inhibitors - inhibit the inhibitory receptors
  • Monoclonal antibodies - anti-CD20 (B-cells), anti-erb2 receptor (block growth receptors), anti-VEGF - stop oxygen and nutrient availability for tumours
  • Soluble mediators - GM-CSF - enhance blood cells - after bone marrow transplant
  • Imiquimod - TLR 7/8 agonist - enhance anti-tumoural/antiviral response
29
Q

Why are tumours hard to vaccinate against?

2 points

A
  • They are very immunosuppressive - switch off immune system

- Lots of normal cells have the same receptors as tumours - don’t want to kill them too

30
Q

Name 4 ways we can overcome tumour suppression? (4 points)

A
  • Activate T cells - blockade inhibitory receptor on T-cells - allows their activation
  • Block IL-10/TGF-beta - adoptive transfer of IL-2 treated cells
  • Up regulate MHC1-IFNgammar treatment
  • Engineer ‘super T cells’ - highly active (Dont require MCH1)
31
Q

Name and describe a novel anti-tumour strategy

1 point

A
  • Dendritic cell vaccination therapy

- Remove DCs - add adjuvants - reinject

32
Q

Explain ‘super’ T cell/Car-T therapy (2 points)

A
  • Engineer antigen binding part of antibody onto T cell receptor
  • Add activatory domains to T cell receptor - which adds many activation signals - as tumours can deactivate T cells
33
Q

Why is antibody-CD3 good? (2 points)

A
  • Is a hybrid - circumvents need for MHC1 for T cell activation
  • So the tumours antigen no longer need to be protein derived
34
Q

How can NK cells be used for treating tumours?

2 points

A
  • Increases the homing and maturation of NK cells - by changing sugars on surface/homing receptors
  • Create CAR receptors - for NK cells
35
Q

Explain host-directed therapy - for infectious disease

3 points - virus, bacteria, fungi

A
  • Doesn’t target pathogen - targets host

Viruses - Uses interferon therapies - Targets host dependent life cycle - unlikely this will mutate - no resistance

Bacteria - e.g., tuberculosis - promotes phagosome maturation - induces antimicrobial peptides - targets inflammatory response and prevents resistance

  • Fungi - statins - reduces cholesterol/ergoesterol
36
Q

What is TGN1412? (1 point)

A
  • It activated all T cells - caused huge inflammation

- Example of immunotherapy going wrong

Immunolgy (8 decks)

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