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Cellular & Molecular Pathology > Cancer immunology & immunotherapy > Flashcards

Cancer immunology & immunotherapy Flashcards

1
Q

what are the four subsets of leukocytes?

A
  • natural killer
  • cytotoxic
  • memory
  • suppressor
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2
Q

what are the functions of Treg cells?

naive CD4+T stimulate these via

A
  • suppresses tumor immunity
  • promotes immune tolerance
  • maintains lymphocyte homeostasis

stimulated via IL-2 + TGFbeta

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3
Q

what are the functions of Th1 cells?

naive CD4+T stimulate these via

A
  • promotes tumor immunity
  • intracellular pathogens
  • drives immunity

stimulated via IL-12

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4
Q

what are the functions of Th2 cells?

naive CD4+T stimulate these via

A
  • extracellular pathogens
  • allergy
  • asthma

stimulated via IL-4

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5
Q

what are the functionc of Th17 cells?

naive CD4+T stimulate these via

A
  • controversial tumor immunity
  • breaks immune tolerance
  • extracellular bacteria
  • autoimmunity

stimulated via TGF-beta + IL-6 + IL-21 (IL-1beta & IL-23)

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6
Q

what type of t cell is pro tumor?

A

regulatory t cells

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7
Q

what are TAMs and what are their functions?

A

Tumor associate macrophages

they secrete factors that support tumor growth
help metastasis, angiogenesis and lymphoangiogenesis
immunosuppression via t cell inactivation, treg cell induction and inhibition of dc maturation

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8
Q

what are myeloid derived suppressor cells (MDSC) and what are their broad functions?

A

newly identified immature myeloid cells that are characterized by the ability to suppress immune responses and expand during cancer, infection, and inflammatory diseases
- Treg cell recruitment
- immune exclusion
- vascular dysfunction
- DC dysfunction

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9
Q

what is IDO?

Indoleamine 2, 3-dioxygenase

A

an intracellular enzyme that initiates the breakdown of tryptophan in the tumor microenvironment

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10
Q

whats the relationship between IDO and immune function?

A

IDO regulates immune function through control of tryptophan levels (removes the fuel needed for immune activity)

in a normal person IDO ensures the immune system does not over respond

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11
Q

what two mechanisms does IDO suppress the immune system?

A
  • suppression of effector T cell activity which signals to stop the immune response
  • promotion of T regulatory cell activity which acts to actively suppress the immune response
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12
Q

what is the relationship between IDO and cancer?

A

tumor cells hijack the immunosuppressive function of IDO by upregulatoing IDO activity and depleting tryptophan in the tumor microenvironment

without tryptophan to fuel the immune cells, cytotoxic T cells starve and immunosuppressive Tregs are upregulated leading to failure of the immune system to respond appropriately to the cancer

IDO expression is upregulated in several types of cancer

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13
Q

what are the clinical implications and interactions of IDO?

A

preclinical studies suggest that targeting the IDO pathway in combination with other potentially complementary immune pathways may be a key strategy to more effectively activate the antitumor immune response

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14
Q

who is William Bradley Coley?

A

an early contributor to the study of cancer immunotherapy - after reading that a patients tumor disappeared after a bacterial infection, he began injecting cancer patients with bacteria (streptococcus poygenes) which worked because it created much needed immune activation

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14
Q

who is William Bradley Coley?

A

an early contributor to the study of cancer immunotherapy - after reading that a patients tumor disappeared after a bacterial infection, he began injecting cancer patients with bacteria (streptococcus poygenes) which worked because it created much needed immune activation

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15
Q

what are the three stages of cancer immunoediting?

A

elimination, equilibrium (tumor dormancy and editing) and escape (tumor growth and promotion)

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16
Q

what are cold tumors?

A

a tumor that is not likely to trigger a strong immune response.
tend to be surrounded by cells that are able to suppress the immune response and keep T cells from attacking the tumor cells and killing them.
usually do not respond to immunotherapy

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17
Q

what are hot tumors?

A

a tumor that is likely to trigger a strong immune response.
often have many molecules on their surface that allow T cells to attack and kill the tumor cells.
usually respond to immunotherapy.

18
Q

what are the 7 broad stages of the cancer immunity cycle?

A

release of cancer cell antigens
cancer antigen presentation
priming and activation
trafficking of t cells to tumors
infiltration of t cells into tumors
recognition of cancer cells by t cells
killing of cancer cells

19
Q

what are the two types of immunotherapy strategies?

A
  • passive: gives the cancer patient antibodies and other agents so that the patient adopts an immune response that has been developed in a test tub
  • active: involves immunization with antigens that stimulate the immune response
20
Q

give examples of active therapies?

A
  • cytokines
  • dendritic cell vaccines
  • modified tumor cell vaccines
  • peptide vaccines
  • dna vaccines
  • chimeric antigen receptor (CAR) t cells
  • immunostimulatory antibodies
  • bispecific antibodies
21
Q

give examples of passive therapies

A
  • direct targeting antibodies
  • t cells
  • nk cells
  • nk t cells
22
Q

what are bispecific antibodies?

A

artificially generated antibody that can recognise two different epitopes, bi specificity. One recognisees t cell & one a tumour cell which can bring t cells close to tumour cells to engage them, capture tumour antigens better and kill them

23
Q

what is stratified medicine?

A
  • aims to identify how our genes or patterns in levels and state of molecules within our bodies, or subtle differences in medical images, could be used to create robust clinical decision making tests for a range of degenerative diseases
24
Q

what are antibody drug conjugates (ADCs)?

A

drugs designed to target specific cancer cells and release a toxic drug into the cancer cell

25
Q

give three immunotherapy strategies against cancer

A
  • non-specific immunotherapies: include cytokines and chemicals that stimulate a general immune response (most likely used as adjuvants to other therapies)
  • monoclonal antibodies: proteins that stick to specific antigens either directly affecting cells or tagging them for destruction
  • vaccines: made from cancer cells, parts of cells or antigens designed to stimulate the immune system to attack a tumor
26
Q

how are DC vaccines made?

A
  1. a patients DCs are removed stimulated and re-infused with a cancer-specific antigen
  2. treated DCs present to other immune cells
  3. activated immune cells primed to recognise the cancer, mature and proliferate
27
Q

give three uses of monoclonal antibodies to treat cancer

A
  • carrrying drugs or toxins to target cells
  • tagging cell for destruction by immune cells
  • blocking signalling pathway to halt growth or proliferation
28
Q

what is oncolytic virus immunotherapy?

A

a type of cancer therapy where a virus is injected into the tumor mass - it transfects the cell and takes over the machinery, viral cells proliferate inside and can rupture the tumour cell. this releases the tumour antigen, creates inflammation and directly kills the tumour cell

29
Q

How do PD-1 blocking antibodies treat cancer?

A

When PD-1 (on tumour specific t cell) binds to PD-L1(on tumour cell), it basically tells the T cell to leave the other cell alone.
Some cancer cells have large amounts of PD-L1, which helps them hide from an immune attack.
Monoclonal antibodies that target either PD-1 or PD-L1 can block this binding and boost the immune response against cancer cells.

30
Q

how do CTLA4 blocking antibodies treat cancer?

A
31
Q

whats the function of CTLA4?

(immune checkpoint protein)

A

CTLA-4 is thought to regulate T-cell proliferation early in an immune response, primarily in lymph nodes
After T-cell activation, CTLA-4 is stored in the intracellular vesicles, and recruited to the immunological synapse formed between T cells and APCs, and inhibits further activation of T cells by blocking signals initiated by T-cell receptors and CD28.

master switch for t cell activation

32
Q

give three of the most successful checkpoint inhibitor antibodies

A
  • Opdivo (nivolumab)= PD-1 inhibitor
  • Keytruda (pembrolizumab)= PD-1 inhibitor
  • Yervoy (ipilimumab)= CTLA-4 inhibitor
33
Q

what occurs in the primary immune resistance stage

A
34
Q

what occurs in the primary immune resistance stage

A
  • low mutational load/ nonn-immunogenic tumour
  • lack of immune recognition (eg absence of DC)
  • immune suppression by cells in the tumor microenvironment
35
Q

what occurs during secondary immune resistance?

A
  • loss of tumor antigen expression or display
  • resistance to immune effector cytokines (eg IFN-gamma)
  • upregulation of other inhibitory molecules/hyperexhaustion
36
Q

what occurs during secondary immune resistance?

A
  • loss of tumor antigen expression or display
  • resistance to immune effector cytokines (eg IFN-gamma)
  • upregulation of other inhibitory molecules/hyperexhaustion
37
Q

what is fecal microbiota transplantation?

A

(FMT) is the administration of a solution of fecal matter from a donor into the intestinal tract of a recipient in order to directly change the recipient’s gut microbial composition and confer a health benefit

38
Q

how can fecal microbiota transplant be used to treat cancer?

A
39
Q

what is adoptive cell transfer? give two examples of therapies

A

A type of immunotherapy in which T cells (a type of immune cell) are given to a patient to help the body fight diseases, such as cancer

examples: tumour infiltrating lymphocytes, chimeric antigen receptor t cell therapy

40
Q

what is Rituximab?

A

the first monoclonal antibody approved for the treatment of cancer
(anti-hHCD20 mAb)

41
Q

what is CAR-T therapy?

A

CAR T-cell therapies are customized for each individual patient. They are made by collecting T cells from the patient and re-engineering them in the laboratory to produce proteins on their surface called chimeric antigen receptors, or CARs.these cells are then expanded and infused back into the patient where they will continue to multply. The CARs recognize and bind to specific proteins, or antigens, on the surface of cancer cells.

42
Q

what patient monitoring is needed after CAR-T therapy?

A

disease response: CT scans, bone marrow biopsies, peripheral blood flow cytometry
CAR T cell persistance: immunohistochemistry of bone marrow biopsies, RT-PCR and flow cytometry of blood and bone marrow aspirate

43
Q

how do non-specific immunotherapies work?
specifically cytokines

A

synthetic cytokines drive groth and proliferation of immune cells
abundant immune cells now target and kill cancer cells

Cellular & Molecular Pathology (12 decks)

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