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Cancer > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What does inflammation protect against?

A

Infectious agents.

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2
Q

What is the role of the epithelium in inflammation?

A

Proliferation, to repair damaged barrier

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3
Q

What is the role of the endothelium in inflammation?

A

Angiogenesis and vasodilation to increase blood flow, increased vascular permeability to provide serum/nutrients for repair.

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4
Q

What is the role of fibroblasts in inflammation?

A

Repair the structure of the damaged tissue.

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5
Q

What is the role of leukocytes in inflammation?

A

Detect damage/infection, initiate inflammation and direct inflammation type, destroy pathogen, regulate other tissue cells, stimulate tissue repair, direct resolution of inflammation.

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6
Q

What detects pathogen-associated molecular patterns (PAMPs)?

A

Toll-like receptors (TLRs)

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7
Q

What are host molecules released from damaged/stressed cells called?

A

Damage-associated molecular patterns (DAMPs)

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8
Q

What detects DAMPs?

A

TLRs

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9
Q

What does TLR stimulation induce?

A

Cytokine and chemokine production and cell differentiation (e.g. dendritic cells).

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10
Q

What do TLRs require for signal transduction?

A

MyD88

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11
Q

What do TLRs, DAMPs, PAMPs and other pattern recognition receptors (PRRs) do?

A

Initiate and potentiate inflammation, influence adaptive responses.

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12
Q

What do cytokines do?

A

Regulate broad aspects of leukocyte function and differentiation.

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13
Q

What do chemokines do?

A

chemoattractans: recruit leukocytes into tissues and control their localisation.

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14
Q

Which cells mediate adaptive immunity?

A

T and B cells.

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15
Q

What do T cell receptors and B cell receptors recognise?

A

Antigens

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16
Q

Which antigens do T cell receptors recognise?

A

Protein derived antigens presented in the context of MHC molecules on the surface of antigen presenting cells.

17
Q

What is an antigen?

A

Any substance that can be recognised by a TCR and/or a BCR. Host-derived or pathogen-derived.

18
Q

What happens to lymphocytes that recognise self antigens?

A

They are destroyed or converted into regulatory T cells. This prevents autoimmune disease.

19
Q

What do dendritic cells do?

A

Pick up and present antigens.

20
Q

Which type of T cells are CD4+ cells?

A

Helper T cells.

21
Q

Which type of T cells are killer cells?

A

CD8+ cells.

22
Q

How does T cell priming work?

A

Dendritic cell activates CD4+ T cells
CD4+ T cells license the dendritic cells.
Dendritic cell then primes CD8+ T cells.

23
Q

What do Naiive B cells become?

A

Memory B cells or plasma B cells.

24
Q

What does the germinal centre reaction do?

A

Increase affinity for antigen.

25
Q

What percentage of cancer deaths are linked to pre-existing infection or inflammation?

A

15-20%

26
Q

Which pro-tumorigenic processes occur in chronically inflamed tissue?

A 
Continuous tissue damage and repair.
Hyperproliferative epithelilum.
Hypoxia disrupts DNA repair.
Inhibition of p53 activity.
Mutagenic products from leukocytes. 
Extensive angiogenesis.
Protease remodelling of the stroma.
Release of stromal growth factor stores.
27
Q

What is MyD88 required for?

A

Signalling through most TLRs, and IL1R.

28
Q

Which molecule is required for liver tumorigenesis?

A

MyD88

29
Q

How does the immune response control early tumours?

A

NK cells recognise and attack early tumour cells.
NK cells and other effectors recruited to site by chemokines.
Dendritic cells head for the lymph node carrying tumour antigens.
Dendritic cells activate tumour specific T cells which home to tumour site. Cytotoxic T cells and Th1 (CD4). Along with macrophages these cells help to eliminate tumour cells.

30
Q

What are the three Es of tumour immunoediting?

A

Elimination
Equilibrium
Escape

31
Q

What are the 6 hallmarks of cancer?

A 
Tissue invasion and metastasis.
Evasion of apoptosis.
Sustained angiogenesis.
Limitless replicative potential.
Self sufficiency in growth signals.
Insensitivity to growth inhibitors.
32
Q

Give three examples of evidence of cancer-associated inflammation.

A
  1. Inflammatory leukocytes in all tumours from very early stages.
  2. Tumours constitutively produce cytokines, chemokines, DAMPs and other pro-inflammatory molecules.
  3. Oncogene activation can induce inflammatory programmes.
33
Q

What controls leukocyte migration?

A

Chemokines.

34
Q

In tumours what causes chemokine receptors to be switched on?

A

Hypoxia.

35
Q

What does TAM stand for?

A

Tumour-associated macrophages.

36
Q

What kind of prognosis does a high number of TAMs correlate with?

A

Poor prognosis.

37
Q

In what way can TAMs help tumour growth?

A

Stimulate cell proliferation and angiogenesis.

Can make immunosuppresive molecules (IL-10, TGFβ).

38
Q

What does VEGF do?

A

Induce angiogenesis.

39
Q

What happens to the macrophages as the tumour progresses?

A

They polarise.

Cancer (11 decks)

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