MI 05b: Tumors and Transplants Flashcards

1
Q

In the case of (tumors/transplants), it’s better to have enhanced immunity.

A

Tumors

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2
Q

In the case of (tumors/transplants), it’s better to have reduced immunity.

A

Transplants

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3
Q

T/F: One of the key issues with tumors is that the immune system doesn’t react to them.

A

False

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4
Q

T/F: Being immunodeficient increases individual’s chances of developing tumors.

A

True

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5
Q

(X) cells recognize tumor antigens. These presented antigens could be products of:

A

X = T

  1. Mutated or over-expressed self protein
  2. Oncogene/tumor suppressor gene
  3. Oncogenic virus
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6
Q

Immune system primarily kills off tumors via (X) cells, presented on (Y).

A
X = CD8 CTL
Y = MHC Class I
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7
Q

Tumor response: Most development/expansion of (X) cells takes place in (Y).

A
X = CD8 CTL
Y = lymph nodes
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8
Q

Tumor response: activation of T cell occurs at which location? This occurs when it recognizes tumor antigen presented via (X).

A

Lymph node;

X = dendritic cell

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9
Q

Tumors can evade immune system in which way(s)?

A
  1. Don’t produce antigen
  2. MHC Class I deficiency
  3. Inhibitory proteins (surface or secreted)
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10
Q

The “immune checkpoints” are (stimulatory/inhibitory) (ligands/receptors) on (X) cell that, under normal conditions, bind (Y).

A

Inhibitory;
Receptors;
X = T
Y = B7 ligands on APC

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11
Q

List the “immune checkpoint” receptors on T cells.

A
  1. CTLA-4

2. PD-1

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12
Q

Tumor cells take advantage of (stimulatory/inhibitory) receptors on T cells. Specifically, the tumor cell expresses (X) to bind (Y), resulting in (Z).

A

Inhibitory;
X = PD-L1
Y = PD-1 receptor
Z = apoptosis of CD8 T cell

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13
Q

T/F: Interaction between PD-1 and PD-L1 ligand prevents interaction between CD28 and B7 ligand.

A

False

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14
Q

How do cancer therapy drugs take advantage of the “immune checkpoint” receptors?

A

Anti-PD-1 antibody blocks PD-1 on T cell, preventing lethal PD-L1 (tumor cell) from binding

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15
Q

Antibodies directed against tumor antigens is an example of (passive/active) immunization.

A

Passive

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16
Q

Vaccination against oncogenic viruses is an example of (passive/active) immunization.

17
Q

Tumor-pulsed dendritic cells is an example of (passive/active) immunization.

18
Q

Blocking growth factor signaling of tumor cells is an example of (passive/active) immunization.

19
Q

“Syngeneic” refers to:

A

Genetically identical individuals

20
Q

“Allogeneic” refers to:

A

Same species, different individuals

21
Q

“Xenogeneic” refers to:

A

Different species

22
Q

In transplant rejection, the donor’s self peptide is a(n) (X) and recognized by (Y) as non-self.

A
X = alloantigen
Y = T cells
23
Q

In transplant rejection, “sensitization” involves presentation of (X) to (CD4/CD8) T cells by (Y) cells in (Z) location.

A

X = alloantigen;
Both CD4 and CD8
Y = dendritic
Z = lymph node

24
Q

Alloantigen recognition by T cells is (direct/indirect), aka presented to T cell via (X).

A

Both;
X = allogenic/donor APC (direct)
OR self-MHC/host APC after uptake and processing (indirect)

25
Hyperacute graft rejection occurs within which time frame? It's primarily a result of (X) recognizing (Y) on (Z) cells.
Minutes; X = recipient Ab Y = antigens Z = endothelial
26
(Chronic/Acute/Hyperacute) graft rejection is primarily result of complement activation and coagulation.
Hyperacute
27
Acute graft rejection occurs within which time frame? It's primarily a result of (active/passive) immune response that's stimulated by (X) and mediated by (Y) cells.
Days/weeks (up to 6 months); Active; X = graft alloantigens Y = Ab and CD4/CD8 T cells
28
In graft rejection, CD8 cells specifically function to (X). And CD4 cells function to (Y).
``` X = directly destroy graft cells Y = secrete cytokines to destroy graft cells ```
29
(Chronic/Acute/Hyperacute) graft rejection is associated with narrowing of blood vessels (arteriosclerosis).
Chronic
30
(Chronic/Acute/Hyperacute) graft rejection is primarily result of CD4 T cell activity.
Chronic (releasing inflammatory cytokines)
31
(Chronic/Acute/Hyperacute) graft rejection has characteristic endothelial damage.
Hyperacute
32
(Chronic/Acute/Hyperacute) graft rejection has characteristic intimal smooth muscle proliferation.
Chronic
33
(Chronic/Acute/Hyperacute) graft rejection has characteristic parenchymal damage.
Acute
34
List the two key methods used to prevent graft rejection.
1. HLA typing (matching) | 2. Immunosuppression
35
In immunosuppression, the most common goal is to block (X) function.
X = T cell
36
CTLA4-Ig is effective treatment for (tumor/transplant rejection). What's the mechanism of action?
Transplant rejection; | Binds B7 and blocks T-cell (CD28) from binding
37
ABO blood antibodies are which Ig class?
IgM
38
Rh blood antibodies are which Ig class?
IgG