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MICR 270 > Module 5: Vaccines and Translational Immunology > Flashcards

Module 5: Vaccines and Translational Immunology Flashcards

1
Q

Immunological techniques

A

-ELISA
-flow cytometry
-monoclonal antibodies

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2
Q

ELISA

A

-bottom of wells coated with antigen specific to antibody you want to measure
-wash
-primary antibody is added and if present will bind to antigens
-wash
-secondary antibody is added and will bind to Fc portion of primary antibodies already present
-wash
-enzyme substrate added to well and produces coloured product if antibodies are present

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3
Q

What does ELISA measure

A

-coloured reaction product by absorbance
-detects presence of antibodies

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4
Q

Flow cytometry

A

-laser light is scattered after being passed through stream of cells
-the way the light is scattered is unique to each cell type

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5
Q

What does flow cytometry measure

A

-used to measure physical properties of a cell or specific antigens in a cell
-can also measure total number of cells in suspension, the type and the overall composition

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6
Q

Clinical application of flow cytometry

A

-can be used to diagnose cancer by detecting DNA aneuploidy

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7
Q

Monoclonal antibodies

A

-created in a lab
-immortal cells that produce unlimited quantities of one identical antibody

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8
Q

What do monoclonal antibodies measure

A

-immunotoxins
-radiolabelled antibodies

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9
Q

Clinical application of monoclonal antibodies

A

-can be produced for defence against specific diseases and cancer

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10
Q

Types of vaccines

A

-live attenuated vaccines
-killed-inactivated vaccines
-toxoid vaccines
-subunit vaccines

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11
Q

Live attenuated vaccines

A

-modified strain of the disease-causing agent which had lost its pathogenic ability
-provides prolonged exposure to disease
-but has a potential to revert to virulent form

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12
Q

Examples of live attenuated vaccines

A

-smallpox
-oral poliovirus
-measles

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13
Q

Killed-inactivated vaccine

A

-contains a strain of the disease causing agent that has been inactivated by heat, chemicals or radiation
-safer option because it cannot mutate to virulent form
-but generally requires multiple booster doses

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14
Q

Examples of killed-inactivated vaccines

A

-rabies
-flu

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15
Q

Toxoid vaccine

A

-contains an inactivated toxin that is a product of the pathogen
-safe because it is not a living organism that can spread
-may require several doses

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16
Q

Examples of toxoid vaccines

A

-tetanus
-diphtheria

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17
Q

Subunit vaccine

A

-contains only a small part or fragment of the disease-causing agent
-safest type and can be used on immunocomprimised, pregnant and elderly people
-usually doesnt give long lasting protection

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18
Q

Examples of the subunit vaccine

A

-hepatitis B

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19
Q

mRNA vaccines

A

-most recent vaccine type

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20
Q

mRNA vaccine production

A

-made in the lab from a DNA template of the virus
-encodes an antigen of the virus and then is administered as a vaccine

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21
Q

mRNA host cell

A

-once inside the body, mRNA enters host cell and uses host cell machinery to produce spike protein

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22
Q

mRNA APC

A

-newly formed spike protein exits cell and is recognized by antigen presenting cell
-then displays antigen on surface of the cell

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23
Q

mRNA immune response

A

-antigen is recognized by T helped cell and initiated immune response

24
Q

Antiviral medications against COVID

A

-polymerase inhibitor
-protease inhibitor

25
Q

Ebola vaccines

A

-uses glycoproteins from ebola and puts them into live attenuated recombinant vesicular stomatis vaccine (VSV)

26
Q

Phases of vaccine developement

A

-lab studies
-preclinical studies
-clinical phase 1
-clinical phase 2
-clinical phase 3
-health canada approval

27
Q

Challenges with vaccine development

A

-cost
-cold chain
-continuous monitoring
-gold standard

28
Q

Challenges with influenza virus development

A

-neuroaminidase antigen
-haemagglutinin antigen

29
Q

Neuroaminidase

A

-surface protein that removes sialic acid from cell surfaces and enables new viral copies to infect spread to other cells

30
Q

Haemagglutinin antigen

A

-binds to sialic acid on cell surface glycoproteins and leads to endocytosis of virus

31
Q

Cancer cell vs normal cell

A

-cancer cells do not need specific growth factors and do not respond to stop signals

32
Q

Tumour

A

-cancer cells continue to grow until forming abnormal masses of tissue

33
Q

Cancer immunotherapy

A

-aimed at enhancing host antitumour immune responses

34
Q

Benign tumour

A

-not cancerous

35
Q

Malignant tumour

A

-cancerous and can metastasize

36
Q

Metastasis

A

-colonization by tumour cells of sites different from primary site of origin

37
Q

Cancer immunity cycle

A

-release of cancer cell antigens: indicate that they are not healthy cells and the immune system is able to recognize the antigens
-cells of the immune system capture them and travel to T cells in lymph nodes
-primary activation: T cells are activated and immune response is initiated
-trafficking of T-cells to tumours: activated T cells move through the blood vessels to site of tumour
-infiltration of T cells: invade tumour to attack it
-recognition of cancer cells by T cells: T cells recognize cancer cells because of antigen they had previously released
-T cells initiate a pathway that results in cancer cell death

38
Q

Immunosurveillance

A

-tumour cells are identified and kept under control by immune system of healthy individuals

39
Q

Immunoediting

A

-elimination
-equilibrium
-escape

40
Q

Cancer immunoediting phase 1

A

-elimination: NK cells, cytotoxic T cells and helper T cells recognize and eliminate tumour cell

41
Q

Cancer immunoediting phase 2

A

-equilibrium: if not eliminated, they enter a state of equilibrium where cell starts to kill immune system
-can last for a short time or for years

42
Q

Cancer immunoediting phase 3

A

-escape: cells are no longer recognized by immune system and can avoid elimination, they can grow uncontrolled and form a tumour

43
Q

Evasion of immune response by cancer cells mechanisms

A

-reduced MHC expression
-poor costimulatory molecules

44
Q

Reduced MHC expression

A

-cancer cells display low levels of MHC on cell surface so that they cannot be recognized

45
Q

Poor costimulatory molecules

A

-tumours lack there so T cells can only be partially activated

46
Q

Advantages of cancer immunotherapy

A

-able to attack cancerous cells throughout all organs in body
-allows immune system to target and eliminate cancer cells without damaging healthy cells resulting in fewer side effects
-takes advantage of immunological memory, allowing for possibility of long term protection
-can be applied to almost any types of cancer

47
Q

Tumour infiltrating lymphocytes (TILs)

A

-prognostic biomarker in some cancers
-can leave blood stream and migrate to infiltrate tumour under the influence of chemokines

48
Q

T cell inflamed “hot” tumours

A

-show higher CD8 TILs and interferon genes
-usually respond well to treatment

49
Q

T cell non-inflamed “cold” tumours

A

-lower CD8 TILs and interferon genes
-usually show an inferior response to treatment

50
Q

Cold tumour treatment

A

-one could convert cold tumours to hot tumours by stimulating tumour interferon activity

51
Q

Immunoscore

A

-measures density/numbers of T cells in the center and at the periphery of the tumour by immunochemistry

52
Q

Immunoscore application

A

-can help stratify patients as having high or low risk cancers and aid in developing treatment plans

53
Q

Immunoscore steps

A

-separate tumour in central and peripheral regions
-stain for T cells and conduct digital pathology
-assign a score to the tumour to relate it with an associated diagnosis or risk attribution

54
Q

Hybridoma cell

A

-perpetual source of antibodies against one antigen
-secrete one identical antibody

55
Q

Immunohistochemistry

A

-how you derive immunoscore

56
Q

VLP (virus like particle) vaccines

A

-composed of viral structural proteins that structurally resemble human papillomavirus (HPV)

MICR 270 (5 decks)

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