Biology 465 > Crowd Control: Basic Tumor Immunology > Flashcards

Crowd Control: Basic Tumor Immunology Flashcards

(48 cards)

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1
Q

What are the two arms of the immune system?

A

Humoral and cellular

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2
Q

What occurs in hypoxic areas?

A
  • monocytes are continually recruited into tumors, differentiated into tumor-associated macrophages (TAMs), and then accumulate in these areas
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3
Q

How to macrophages respond to the levels of hypoxia in tumors?

A

They upregulate the TF hypoxia-inducible factors 1 and 2

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4
Q

What does Hypoxia-inducible factors 1 and 2 activate? What is significant about this?

A
  • A broad array of mitogenic, proinvasive, proangiogenic, and prometastatic genes
  • Possible explanation of why high numbers of TAMs correlate with poor prognosis in various forms of cancer
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5
Q

In environments with LPS/INF-gamma, what type of TAM is present and what does it effect?

A

Anti-tumor TAM

  • cytokines (eg., immunostimulatory)
  • chemokines (eg., for lymphocytes)
  • tumor cell lysis
  • reactive oxygen and nitrogen species
  • metalloproteinases (MMP-7,9 and 12)
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6
Q

In hypoxic environments, what type of TAMs are present and what do they effect?

A

Pro-tumor TAMs

  • pro-angiogenic cytokines and enzymes
  • reactive oxygen and nitrogen species
  • cytokines (mitogens and immunosuppresive factors)
  • tissue factor/uPA
  • metalloproteinases (wide range)
  • chemokines (eg., monocytes and macrophages)
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7
Q

What happens when there is in an increase in IL-10 concentration in hypoxic environments?

A

It is the autoinflammatory cytokine that attempts to heal the wound

  • it brings iron, VEGF and other GF
  • the brought iron feeds the proliferating cells
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8
Q

What are Anti-tumour macrophages (MACs) capable of?

A
  • Anti-infection and phagocytic capable
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9
Q

In normal cells, what do Pro-tumor TAMs do?

A

They assist in wound healing

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10
Q

How are MACs and TAMS different in what they respond?

A

What they respond to:

  • MACs: respond to LPS or INF-gamma and phagocytize an infectious pathogen or tumour cell
  • TAMs: responds to hypoxia in an attempt to solve the problem
  • > chronic infection attracts wound healing TAMs
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11
Q

How are MACs and TAMS different in their cytokines?

A

Cytokines:

  • MACs: cytokines are immuno-stimulatory
  • TAMs: proangiogenic (eg., IL-10 stimulates HIF1alpha and VEGF)
  • > pro-angiogenesis promotes cell survival
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12
Q

How are MACs and TAMS different in what their cytokines or chemokines attract?

A

Chemokines/cytokines:

  • MACs: their chemokines attract just enough T helper lymphocytes to protect from infection or tumor cells
  • TAMs: cytokines are anti-inflammatory work in combination with immuno-suppresive compounds
  • > immunosuppression promotes unusual cell survival
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13
Q

How are MACs and TAMS different in their ROS release?

A

ROS release:

  • MACs: tolerable level, easily controlled
  • TAMs: too high a level, contributes to tissue injury, DNA damage and genomic instability
  • > high levels of ROS promotes genomic instability
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14
Q

How are MACs and TAMS different in their treatment of the issue?

A

Issue treatment:

  • MACs: releases TNF-alpha at local levels that induces apoptosis in possible cancerous cells
  • TAMs: recruited to tumor environment by tissue factor and chemokines
  • > TAMs usually indicate an unresolved chronic infection that are immunosuppressive and tumor supportive
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15
Q

How are MACs and TAMS different in their MMPs?

A

MMPs:

  • MACs: 7, 9 and 12 -> remove potentially cancerous and unusual cells by phagocytosis
  • TAMs: involved in the enhanced mobility and metastatic capacity of tumor cells
  • > increases metastatic capacity
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16
Q

Why is the diversity of recognition possibilities for TCRs is not limited by the linear genome?

A

T cells can rearrange their DNA during development to an enormously wide range of recognition

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17
Q

What is the estimated recognition diversity?

A

10^15

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18
Q

What occurs to potentially dangerous T and B cells that have self reactive receptors?

A

They are eliminated by negative selection in the thymus and bone marrow respectively

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19
Q

What do cytotoxic T cells (CTLs) develop on their surface?

A

They develop antibody like molecules on their surface (T cell receptors) that display and Ag “like” recognition for a specific pathogen

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20
Q

What is released when a CTL uses its TCR to recognize and bind its target cell?

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A

Cytotoxic granules are released into the cell (eg., granzymes), as well as FasL binding (-> caspase-8 activation) to induce apoptosis in the target cell

21
Q

How do Ag-presenting cells work?

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A
  • antigens are taken up by Langerhans cells in the skin
  • Langerhans cells leave the skin and enter the lymphatic system
  • Langerhans cells enter the lymph node to become dendritic cells expressing B7 (CD80)
  • B7-positive dendritic cells stimulate naive T cells
22
Q

What occurs in antigen presenting cells after phagocytosis of foreign bodies?

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A

Antigen presenting cells move the foreign bodies to the surface with MHC class II receptors

23
Q

Which cells is MHC class I expressed on?

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A

All cells, used for normal cell recognition

24
Q

Where do immunocyte encounters occur?

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A

Within the lymph nodes

25
Explain a productive interaction between APC and T helper cell.
- APC presents the unusual epitope on its MHC II which is recognized by a TCR on a TH cell - the TH cell is activated and displays more TCR which can go an activate naive B cells - the B cells differentiate into plasma cells and then release Ab
26
What is a unproductive interaction between a dendritic cell and a TH cell?
The molecular architecture displayed was not a match for the MHC class II presentation
27
How is an antigen taken up by an APC?
By phagocytosis, pinocytosis, or endocytosis
28
How is a T cell activated?
Once an antigen is presented by an APC through its MHC, a second signal is provided via CD80/86-CD28 that induces the expression of CD154 and CD152 later on - T cell CD154 binds with CD40 on APCs - this interaction induces the activation and proliferation of downstream effector cells
29
How are T cells inactivated?
CD152 (expressed 48-72 hours after T cell activation) will preferentially bind to CD80/86 on APCs because of its higher affinity, displacing CD28 and in turn suppresing T cell activity
30
What two signals are required for T cells to activate?
1. The TCR expressed antigen specific receptor BINDs to antigenic peptide held by the MHC complex 2. The APC CD80/86 BINDs to T cell CD28
31
What does the two necessary signals lead to in both TH and TC cells?
Leads to T cell proliferation, and increased release of IL-2, and increased expression of Bcl-xL
32
How do TC cells get directly activated to become cytotoxic?
TH cell binding of CD154 to APC CD40 licences the APC to directly activate them - also can be done by cytokines, LPS, viruses or other other inflammatory stimuli
33
When and how is the negative control provided?
- provided after 48 to 72 hours of activation | - caused by the increased expression of CD152 that binds to CD80/86 on APCs displacing CD28 binding
34
How is TC activity suppressed?
Bcl-xL is downregulated which induces apoptosis
35
How does a cell display an intracellular Ag by MHC class I molecules?
- the intracellular protein is degraded into peptide fragments by the proteasome - binds to the MHC class I which moves to the cell surface in a vesicle - > ends up on the plasma membrane to display - all cells display Ag on their surface with MHC class I molecules
36
How do helper T cells activate cytotoxic T cells?
- TH (CD4+) can activate CTLs that can use their TCRs to recognize and bind Ag presented on the cell surface of many cell types by MHC class I recognition - > attacks the Ag displaying cell
37
What do cytotoxic T cells use to attack the Ag displaying cells?
- perforin - granzyme - FasL
38
What is the mechanism of CTLs?
- TC displays FasL on its cell surface which binds to the target cell's Fas receptors - The Fas receptor dimerizes which allows FADD, pro-caspase 8 and pro-caspase 3 to bind - FADD activates which activates the pro-caspases thus resulting in apoptosis
39
What does CTL killing utilize?
Utilizes extrinsic apoptotic mechanisms
40
Why would a NK cell attack a cancer cell?
MHC class I was expressed which is recognized as being irregular (including level of expression) - extensive damage occurs after 60 min of attack - damage similar to apoptosis
41
What is a key attractant for monocytes and macrophages?
Some tumors release colony stimulating factor-1 (CSF-1) | - monocytes and macrophages won't infiltrate if there is a CSF knockout -> cannot express CSF-1
42
Is HIF1-alpha increased or decreased in hypoxic areas?
Increased
43
Where can VEGF be expressed from?
- the tumor | - the macrophages within the tumor
44
What happens when you admix normal stromal fibroblasts with breast cancer cells before injection?
There is no induction of abundant vascularization
45
What happens when you admix carcinoma-associated fibroblasts (CAFs) with breast cancer cells before injection?
It induces abundant vascularization
46
In the elimination phase of cancer immunoediting, what occurs?
- Cancer immunosurveillance - more immunological control than cancer progression - there is protection provided by innate and adaptive immune cells
47
In the equilibrium phase of cancer immunoediting, what occurs?
- Cancer persistence - equal immunological control vs. cancer progression - there is a constant cycle of genetic instability and immune selection
48
In the escape phase of cancer immunoediting, what occurs?
- Cancer progression - More cancer progression than immunological control - the progression inhibits the ability of the immune cells
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