cancer immunity Flashcards

1
Q

what cells give a good prognosis

A

CD8+ cells, TLS and M1

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2
Q

what cells give a bad prognosis

A

M2 and Treg due to a immunosuppressive role

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3
Q

what is the function of the antigen processing machinery

A

that proteins of the cell are destroyed into smaller peptides and get loaded onto HLA/MHC class 1 which presents the peptides to the CD8 T cel

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4
Q

oncofoetal proteins

A

proteins that are normally expressed during embryology but are now being expressed by the tumor

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5
Q

neo antigen

A

somatic mutation has lead to the making of non self proteins or antigens

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6
Q

cross presentation

A

dendritic cells load peptides/antigens derived from exogenous route onto HLA class 1 molecules

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7
Q

what happens in the main killing pathway when a CD8+ cytotoxic T cell binds to a transformed cell

A

the t cell will start to produce perforin and granzyme B which will produce pores in the cell membrane of the bad cell and cause apoptosis

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8
Q

explain FAS-FASL interaction

A

this is the non main pathway of killing a transformed cell by T cell. FAS-FASL will interact and activate caspase 8 which will active caspase cascades and this will lead to cell death

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9
Q

why are anti tumor immune responses desirably dominated by TH1 type CD4 responses

A

because these will produce pro inflammaitory cytokines like IL12 and IFN-y which will promote tumor immunity.

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10
Q

which signals proliferate T0 cells into Treg cells

A

TGF-B and IL-2

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11
Q

in which two pathways can a tumor escape the immune system

A

PD-L1 expression in tumor

immune suppresed microenvironmend

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12
Q

explain the working of PD-L1

A

PD-L1 is a ligand that binds and transmits a negative signal to T cells which causes T cells to become inhibited. the effect is loss of HLA/MHC class 1

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13
Q

what normaly happens when MHC class1 is lost

A

NK cells will recognize that MHC class 1 is lost and cause lysis. however this is dependend on ligands in the tumor, these ligands can be lost and then the NK will not come into action

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14
Q

what are tumours with a high mutation rate

A

polymerase mutatns (POLE) and mismatch repair deficient tumours

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15
Q

which tumours often have a HLA class 1 defect

A

MMRdeficient tumours

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16
Q

how does IL2 therapy work, what are downsides to this therapy

A

you will activate T cells, high toxicity and not cancer specific

17
Q

how does TIL therapy work and what are downsides to this therapy

A

tumour antigens are grown. downsides are time/costs and highly dependent on in vitro manipulation

18
Q

how do neoantigen targeted therapies work, what are downsides

A

mutation in tumor is detected and then vaccinated against. usage of gene sequencing. downsides are high costs and time

19
Q

how do antigen therapies tumor associated proteins work

A

e.g. GP100 glycoprotein enriched in melanocytes, vaccination against this specific protein. downside is limited efficacy

20
Q

how does checkpoint blockade work

A

PD-L1 is on the APC and PD-1 on the T cell. you can block PD-1 on the T cell and then you will block the negative signal and thus elimination of the cell can occur.