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MEDSCI302 > 28 Cancer Immunology II > Flashcards

28 Cancer Immunology II Flashcards

(58 cards)

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1
Q

NAME 3 lines of evidence for immune SURVEILLANCE

A
  • Immunosuppressed patients = INC tumors
  • Nude mice
  • RAG-/- mice
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2
Q

WHY do immunosuppressed patients show INC tumor?

A

“ACCEPT” tumors

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3
Q

What is special about NUDE mice

A

No thymus

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4
Q

Are nude mice a good model of immunedeficiency?

Explain

A

NO

  • Has functional T-cells
  • Has more NK cells than normal mice
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5
Q

What is RAG2

A

Lymphocyte genetic RESHUFFLING gene

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6
Q

What happens in RAG2-/- mice?

A

100% TUMOR development

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7
Q

Define immunoediting

A

Immune system driving expansion of tumors

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8
Q

What are the 3 E’s of immunoediting?

A

Elimination
Equilibrium
Escape

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9
Q

What happens in the elimination step

A

Immune cells DESTROY cancer cells 😃

only have some mutations = slightly immunogenic

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10
Q

What happens in the EQUILIBRIM stage

A

Some cells undergo FURTHER mutation
= RESISTANT to immune killing 😭
(Immune system selects FOR resistance)

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11
Q

What happens in the ESCAPE stage

A

EXPANSION of immune-RESISTANT cells (highly mutated)

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12
Q

Acronym for the ESCAPE mechanisms in tumor cells?

List these

A 
HCTI
“Hiding”
Counterattack
T-cell dysfuncion
Immunosuppression
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13
Q

NAME 2 ways of “hiding” from immune system

A
  • MHCI down-reg or KO

* NK killing evasion

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14
Q

Function of normal MHCI?

What binds to MHCI?

A

ALL cells present proteome antigens on MHCI

LYMPHOCYTES perform immune surverillance

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15
Q

What is the EFFECT of KO MHCI

A

No MHCI = no antigen presentation = NO CD8 cytotoxic T-cell killing

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16
Q

2 ways in which tumor cells EVADE NK cell killing?

A

Secreting INHIBITORY signals (TGFβ, PGE2) = ⬇️NK RECEPTORS

Down-reg co-stimulatory B7 = ⬇️NK ACTIVITY

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17
Q

What happens in MELANOMA with INC B7 activity?

A

INC B7 = INC NK activity = tumor free!!

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18
Q

What is B7

A

Co-stimulatory molecule for NK cells

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19
Q

3 ways in which tumor cells perform COUNTERATTACK

A
  1. CHECKPOINT inhibition
  2. APOPTOTIC escape
  3. Fas-pathway KILLING
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20
Q

How do cancer cells inhibit immune CHECKPOINTS

A

Cancer cells have PD-L1 (finger), which binds T-cell PD1 (button)
= INHIBIT T-cell signalling
= APOPTOSIS

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21
Q

How do cancer cells EVADE apoptosis?

A

Down-regualte apoptotic PROTEINS

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22
Q

In the Fas pathway, which cell DIES?

  • cell with Fas-R
  • cell with Fas-L
A

Cell with Fas-R will die

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23
Q

How do cancer cells kill T-cells via FAS pathway?

A

Fas-L (cancer cells) binds Fas-R (CTLs)

= counterattack to KILL CTLs

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24
Q

How does HIGH CD8 T-cell infiltration usually affect PROGNOSIS?

Study These Flashcards
A

BETTER prognosis

25
2 ways tumor cells cause T-cells DYSFUNCTION
* Impair T-cell SIGNALLING | * Impair NF-kB signalling
26
How do tumor cells impair T-cell SIGNALLING?
Tumor secretes factors to ∆signal transduction
27
Is the ∆signal transduction in T-cells reversible? | Explain
Usually reversible if: * T-cell REMOVED from tumor microenvironment * EXCISION of tumor
28
Where does impaired T-cell signalling BEGIN? | How does it progress?
Begins AT tumor site | Spreads to PERIPHERAL T-cells
29
Why does impaired NF-kB signalling cause T-cell dysfunctin
NF-kB is a TF that inducdes many IMMUNE GENES
30
Name 2 Tx approches to REPLACE T-cells
1. Transplant cells | 2. “Designer” T-cells
31
In a mouse study, lymphocytes to be transplanted were cultured with WHAT factor? Why?
Lymphocytes from HEALTHY mice cultured with IL-2 (induces proliferation)
32
What happened when lymphocytes from HEALTHY mice were transplanted to the cancerous mouse?
CURED tumors in mice!
33
Is this transplant method viable in HUMANS?
Only works in 10% of human patients...
34
Name the TYPE of “designer” T-cell
CAR T-cells | = Chimeric Antigen Receptor
35
What are the components of a CAR
Antibody variable region | TcR
36
Benefits of a CAR lymphocyte?
INDEPENDENT antigen recognition = POTENT | does not require MHC or additional co-stimulation!
37
2 PATHWAYS to cause immunosuppression?
Cellular | Soluble
38
Name the 3 cellular methods of inducing immunosuppression
Treg MDSCs TAMs
39
How can tumor cells use Treg cells to cause immunosuppresion?
Promote maturation of NAIVE Treg cells OR Directly stimulate MATURE Treg cells
40
What are MDSCs
Myeloid-Derived Stem Cells
41
Function of MDSCs
Same as Treg (also suppresses T-cell function)
42
3 things secreted by MDSCs
O2 radicals Arginase 1 iNOS
43
What does Arginase-1 from MDSCs do?
Depletes L-Arginine (needed by T-cells)
44
What does iNOS do?
Inducible NO synthase = makes NO
45
What happens to the NO made by MDSCs?
NO combines with O2 radicals | = peroxynitrite
46
How do MDSCs use peroxynitrite to kill T-cells?
MDSCs present antigens to T-cells | Release TOXIC peroxynitrite = KILL T-cells
47
TAM infiltration = _____ prognosis
BAD prognosis
48
What are the 2 PHENOTYPES of macrophages? | How does this CHANGE in tumors?
``` M1 = ANTI-tumor M2 = PRO-tumor ``` Tumors covnert TAMS to M2 phenotype
49
Name PRO-tumor functions of M2 macrophages
* Invasion (proteases) * Angiogenesis * Proliferation * Immunosuppression
50
What factors are secreted by M2 macrophages to cause immunosuppression?
PD-L1 IDO1 IL10 (induces Treg cells)
51
What is a SOLUBLE immunosuppression method?
IDO1
52
Name 2 PHYSIOLOGICAL functions of IDO1
* INFLAMMATION = normal immunosuppression to allow HEALING | * PREGNANCY = immune TOLERANCE of baby
53
What metabolic PATHWAY is IDO1 part of?
KP = Kyurenine pathway
54
What does INC IDO1 in cancer lead to?
Promote Kyurenine pathway = 95% Tryptophan (W) depletion = accumulation of W metabolites = T-cell APOPTOSIS
55
What is the “Double Trouble” effect caused by KP?
DEC Tryptophan | INC Kyurenine
56
How does the “Double Trouble” effect cause immunosuppresion | DIRECTLY and INDIRECTLY
Directly suppress T/NK cells | Indirectly suppress T/NK cells via ⬆️Treg
57
HIGH IDO1 + Kyurenine = ______ prognosis
POOR prognosis
58
What 2 drug types used in COMBO Tx gives better outcome?
Checkpoint-inhibitor (anti-PD-L1) IDO1-inhibitor Works better as COMBO than alone

MEDSCI302 (8 decks)

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