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Immunology and Haematology > Immunotherapy > Flashcards

Immunotherapy Flashcards

1
Q

What are different kinds of immunotherapies?

A
  • Immune suppressive therapies
    • General suppression
    • Transplant rejection
    • Passive infusion
  • Cytokine therapies
  • Directed antibody therapy
    • Monoclonal vs polyclonal
  • Checkpoint inhibitors
  • Cellular immunotherapy
    • T cells
    • Dendritic cells
    • CAR-T cells
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2
Q

What does ‘blanket’ immune suppresion mean?

A

‘Blanket’ immune suppression means suppressing the entire immune system, risk of opportunistic infections:

  • Need to develop tailored therapies that target specific part of immune system
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3
Q

What is the main risk of ‘blanket’ immune suppresion?

A

Opportunistic infections

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4
Q

Acute rejection is associated with what?

A

Acute rejection is associated with T cell responses that mediate immune cell infiltration into graft:

  • Anti-rejection drugs massively increased graft survivability
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5
Q

How can T cell activation be inhibited?

A

Methods for inhibiting T cell activation to treat graft rejection, done by stopping them from producing IL-2:

  • Cyclosporin
    • Mechanism – targets calcinerin, effecting IL-2 production
  • Rapamycin
    • Mechanism - targets mTOR, affecting IL-2 uptake by T-cell
  • Antibody treatment
    • Mechanism - targeting costimulation
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6
Q

What are some drugs that inhibit T cell activation?

A
  • Cyclosporin
    • Mechanism – targets calcinerin, effecting IL-2 production
  • Rapamycin
    • Mechanism - targets mTOR, affecting IL-2 uptake by T-cell
  • Antibody treatment
    • Mechanism - targeting costimulation
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7
Q

Describe the mechanism of Cyclosporin?

A
  • Mechanism – targets calcinerin, affecting IL-2 production
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8
Q

Describe the mechanism of:

  • cyclosporin
  • rapamycin
  • antibody treatment
A
  • Cyclosporin
    • Mechanism – targets calcinerin, affecting IL-2 production
  • Rapamycin
    • Mechanism - targets mTOR, affecting IL-2 uptake by T-cell
  • Antibody treatment
    • Mechanism - targeting costimulation
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9
Q

What are the different types of immunity?

A
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10
Q

Contrast active and passive immunity?

A
  • Active immunity
    • Person infected or vaccinated with microbe
    • Few days or weeks later individual makes potent adaptive immune response with T cells and antibodies
    • Recovers from challenge with specificity and memory
  • Passive immunity
    • Serum given to patient (from immune individual)
    • Infection and recovery with immunity
    • Specificity but no memory
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11
Q

For active and passive immunity do they have:

  • specificity
  • memory
A
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12
Q

What are examples of passive immunity?

A
  • Snake or spider bites, scorpion or fish stings
    • Passive infusion of antibody specific for toxin
  • Hypogammaglobulinaemia
    • Primary or secondary infusion of IgG to reduce infection
  • Rabies immunoglobulin
    • Post-exposure prophylaxis together with vaccination
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13
Q

What are examples of things immunoglobulins for post-exposure prophylaxis can be used?

A
  • Human normal immunoglobulin (HNIG)
    • Hepatitis A
    • Measles
    • Polio
    • Rebella
  • Specific immunoglobulins
    • Hepatitis B
    • Rabies
    • Tetanus
    • Varicella-zoster virus
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14
Q

What is IV immunoglobulin?

A

A biologic for primary and secondary immune deficiencies:

  • Plasma derived IgG used for replacement therapy
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15
Q

What are indications for IV immunoglobulin?

A
  • Some autoimmune disorders
  • Primary and secondary immunodeficiency’s
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16
Q

What are the different types of immunotherapy?

A
  • Direct (targeted)
    • Antibodies detect an antigen on tumour and destroy target by recruiting immune cells or delivering a toxin or radioisotope to it
    • Target is the tumour
  • Indirect
    • Immune system activated, allowing it to seek and destroy tumour cells
    • Target is the immune system
17
Q

What is direct (targeted) immunotherapy?

A
  • Antibodies detect an antigen on tumour and destroy target by recruiting immune cells or delivering a toxin or radioisotope to it
  • Target is the tumour
18
Q

What is indirect immunotherapy?

A
  • Immune system activated, allowing it to seek and destroy tumour cells
  • Target is the immune system
19
Q

What are examples of direct and indirect immunotherapy?

A
  • Direct
    • Monoclonal antibodies
    • Chimeric antigen receptors (CAR-T cells)
    • Bi-specific antibodies
  • Indirect
    • Tumour vaccines
    • Dendritic cell vaccines
    • Adoptive cell transfer
    • Cytokine therapies
    • Checkpoint inhibitor therapies
    • Stimulatory antibodies
20
Q

For cytokine therapy:

  • drugs
  • effect
  • indication
A

Drugs:

  • Pegylated IFN-a
  • IL-2
  • GM-CSF

Effect:

  • Immunomodulatory cytokines to activate anti-tumour immunity

Indications:

  • Specific cancers
21
Q

What is the difference between polyclonal and monoclonal antibodies?

A

Immunisation with antigen will typically lead to polyclonal response:

  • Many different B cell clones generate antibodies specific for the antigen
  • But a number of epitopes will be bound by antibodies
    • Antibodies with different variable regions bind multiple epitopes

Monoclonal immune response is where a single antibody producing clone produces antibodies:

  • Recognise only one epitope
22
Q

What are different product types of therapeutic antibodies?

A
  • Human (most common)
  • Humanised
  • Chimeric
    • Mixture of mouse and human
  • Fragment
  • Murine
23
Q

What are examples of therapeutic antibodies?

A
  • Rituxan (rituximab)
    • Indication – originally developed for NHL and lymphoma, now found to benefit rheumatoid arthritis
    • Mechanism – specific for the CD20 molecule on cell surface of small population of B cells, allowing immune system to kill it such as macrophages, compliment system and NK cells
  • Infliximab
    • Effect – anti-TNF therapy
    • Mechanism – chimeric antibody blocks function of tumour necrosis factor alpha (TNF), which is a pro-inflammatory cytokine that stimulates an acute phase reaction
    • Indications – rheumatoid arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis
  • Herceptin, also called trastuzumab
    • Mechanism – antibody binds HER2 on cancer cells and marks them for destruction by immune system
    • Indication – HER2 positive metastatic breast cancer
  • Risankizumab
    • Mechanism – targets cytokine associated with inflammatory response underlying plaque psorisasis
    • Indication – plaque psoriasis
24
Q

For rituxan (rituximab):

  • indication
  • mechanism
A
  • Indication – originally developed for NHL and lymphoma, now found to benefit rheumatoid arthritis
  • Mechanism – specific for the CD20 molecule on cell surface of small population of B cells, allowing immune system to kill it such as macrophages, compliment system and NK cells
25
Q

For infliximab:

  • effect
  • mechanism
  • indications
A
  • Effect – anti-TNF therapy
  • Mechanism – chimeric antibody blocks function of tumour necrosis factor alpha (TNF), which is a pro-inflammatory cytokine that stimulates an acute phase reaction
  • Indications – rheumatoid arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis
26
Q

For herceptin:

  • mechanism
  • indication
A
27
Q

For risankizumab:

  • mechanism
  • indication
A
28
Q

What is the effect of checkpoint inhibitors?

A
  • Antibodies that unlocks the adaptive immune response so it can kill the cancer
29
Q

What are the 2 types of checkpoint inhibitors?

A
  • Anti-CTLA4 antibodies
    • Mechanism - normally dendritic cell presents antigen from target cell with MHC, TCR on T cell binds to this and activates T cell. But the B7 part of the dendritic cell also needs to bind with CD28 of T cell for full activation, if B7 binds with CTLA-4 this causes inhibitor effect
  • Anti-PD-1/PD-L1
    • Mechanism - Tumour expresses high levels of PD-L1 which binds to PD-1 on T cell, inhibiting it and tricking it. This blocks this from happening
30
Q

Describe the mechanism of anti-CTLA4 antibodies?

A
  • Mechanism - normally dendritic cell presents antigen from target cell with MHC, TCR on T cell binds to this and activates T cell. But the B7 part of the dendritic cell also needs to bind with CD28 of T cell for full activation, if B7 binds with CTLA-4 this causes inhibitor effect
31
Q

Describe the mechanism of anti-PD-1/PD-L1 antibodies?

A
  • Mechanism - Tumour expresses high levels of PD-L1 which binds to PD-1 on T cell, inhibiting it and tricking it. This blocks this from happening
32
Q

Describe the process of dendritic cell vaccines?

A
  1. Take blood sample from patient
  2. Culture cells in vitro
  3. With cytokines promote APC function
  4. Transfuse patients with APC after uptake of tumour antigen
33
Q

What does ACT stand for?

A

Adoptive cell transfer

34
Q

Describe the process of ACT?

A
  1. Take tumour cells from patient
  2. Assay for specific tumour recognition
  3. Select and expand to billions of cells
  4. Reinfuse post lymphodepletion
35
Q

What is CAR-T cell therapy?

A

CAR T cells are engineered to express antigen-targeted receptors specific for tumour antigens:

  • CAR includes an antigen-binding domain fused to a transmembrane domain followed by T-cell activation domains associated with the T-cell receptor
  • T cell modified with CAR is endowed with a new antigen specificity, supporting T cell activation and killing target cell
36
Q

What does CAR stand for?

A

Chimeric antigen receptors

37
Q

How many generations of CAR are there, and what does each generation add?

A
  • 1st generation
  • 2nd generation
  • 3rd generation

Immunology and Haematology (23 decks)

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