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Biology 465 > Crowd Control: Basic Tumor Immunology > Flashcards

Crowd Control: Basic Tumor Immunology Flashcards

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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?

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?

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?

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?

A

All cells, used for normal cell recognition

24
Q

Where do immunocyte encounters occur?

A

Within the lymph nodes

25
Q

Explain a productive interaction between APC and T helper cell.

A
  • 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
Q

What is a unproductive interaction between a dendritic cell and a TH cell?

A

The molecular architecture displayed was not a match for the MHC class II presentation

27
Q

How is an antigen taken up by an APC?

A

By phagocytosis, pinocytosis, or endocytosis

28
Q

How is a T cell activated?

A

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
Q

How are T cells inactivated?

A

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
Q

What two signals are required for T cells to activate?

A
  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
Q

What does the two necessary signals lead to in both TH and TC cells?

A

Leads to T cell proliferation, and increased release of IL-2, and increased expression of Bcl-xL

32
Q

How do TC cells get directly activated to become cytotoxic?

A

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
Q

When and how is the negative control provided?

A
  • 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
Q

How is TC activity suppressed?

A

Bcl-xL is downregulated which induces apoptosis

35
Q

How does a cell display an intracellular Ag by MHC class I molecules?

A
  • 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
Q

How do helper T cells activate cytotoxic T cells?

A
  • 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
Q

What do cytotoxic T cells use to attack the Ag displaying cells?

A
  • perforin
  • granzyme
  • FasL
38
Q

What is the mechanism of CTLs?

A
  • 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
Q

What does CTL killing utilize?

A

Utilizes extrinsic apoptotic mechanisms

40
Q

Why would a NK cell attack a cancer cell?

A

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
Q

What is a key attractant for monocytes and macrophages?

A

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
Q

Is HIF1-alpha increased or decreased in hypoxic areas?

A

Increased

43
Q

Where can VEGF be expressed from?

A
  • the tumor

- the macrophages within the tumor

44
Q

What happens when you admix normal stromal fibroblasts with breast cancer cells before injection?

A

There is no induction of abundant vascularization

45
Q

What happens when you admix carcinoma-associated fibroblasts (CAFs) with breast cancer cells before injection?

A

It induces abundant vascularization

46
Q

In the elimination phase of cancer immunoediting, what occurs?

A
  • Cancer immunosurveillance
  • more immunological control than cancer progression
  • there is protection provided by innate and adaptive immune cells
47
Q

In the equilibrium phase of cancer immunoediting, what occurs?

A
  • Cancer persistence
  • equal immunological control vs. cancer progression
  • there is a constant cycle of genetic instability and immune selection
48
Q

In the escape phase of cancer immunoediting, what occurs?

A
  • Cancer progression
  • More cancer progression than immunological control
  • the progression inhibits the ability of the immune cells

Biology 465 (15 decks)

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