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biology of cancer > Immune surveilance > Flashcards

Immune surveilance Flashcards

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1
Q

how are cancer cells different from normal cells?

A
  • rapid uncontrolled growth
  • increase mobility
  • invade tissue
  • evade immune system
  • metastasise
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2
Q

what can immunodeficieny lead to?

A

tumor formation; kaposi sarcoma, lymphoma

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3
Q

what can inflammatory conditions lead to?

A

cancers; ulcerative colitis and colon cancer

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4
Q

what was research into how the body can defend against cancer?

A

skin sarcomas in mice induced by chemical carcinogen (methylcholanthrene) showed that:
- anti tumor immune response by CD8+
- production of immune memory
- specificity of individual tumors
= presence of tumor antigens

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5
Q

adaptive immune response

A

involves specialised immune cells and antibodies that attack and destroy foreign invaders and retain memory antigens

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6
Q

what are the immune system’s 3 major ways of preventing tumors

A
  • speedy resolution of inflammation
  • elimination of viral infections
  • early elimination of tumor cells before they can do harm
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7
Q

what is tumor immunosurveillance?

A

process by which immune system, e.g. lymphocytes, continually recognise cancerous and pre-cancerous cells = to their elimination before they can cause damage

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8
Q

tumorigenesis

A
  • normal cells undergoing change
  • develop abnormal tumor antigens
  • danger signals such as extra cellular matrix products
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9
Q

immunoediting; elimination

A
  • NK, NKTs, Macs and DCs (innate)
  • INFy & chemokines = tumor death
  • tumor specific DCs activate adaptive immunity in draining lymph nodes
  • tumor specific CD4+ and CD8+ T cells join
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10
Q

immunoediting; equilibrium

A
  • elimination phase is incomplete
  • tumor cells lie dormant and may modulate tumor antigen expression and stress signals
  • immune system eliminates susceptible tumor clones when possible sufficient to prevent tumor expansion
  • tumor heterogeneity resulting in ‘Darwinian selection’
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11
Q

what are some features of tumor stem cells?

A
  • can evade host immune surveillance
  • tumor seeds
  • lose MHC class1 and have no NK activating ligands and silence TAA. May als downregulate b2m
  • can produce immunosuppressive cytokines
  • selectively recruit ‘reglatory cells’
  • resistant to innate and adaptive immune response
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12
Q

immunoediting; escape

A

immune system unable to control tumor growth = tumor progression

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13
Q

what do some tumor cells express?

A
  • MHC class I/peptide complexes
  • ligands to CD8+ T cells = activation and destruction of the tumor cell
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13
Q

how are CD4+ t cells activated?

A

APCs take up cell debris from tumor cells
- pinocytosis
- receptor mediated endocytosis

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14
Q

how do activated CD4+ T cell exert antu tumor properties?

A
  • lymphotaxin secretion resulting in direct tumor cell death
  • secretion of cytotoxins activating other cells such as; NK, macrophages, CD8+ T cells
  • rarely; tumors themselves can act as APCs by presenting antigens on MHC class II molecs.
    Seen in some melanomas.
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15
Q

process to present on MHC

A

TH1 cytokines:
IL2 > CTL proliferation
IFNy, TNF > MHC I increase on tumor to enhance kill

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16
Q

what are tumor antigens?

A
  • produced by tumor cells & can trigger immune response
  • important in tumor identification and targeting in immunotherapy
17
Q

tumor specific antigens

A

produced only by tumor cells

18
Q

tumor associated antigens

A

produced by tumor cells but also produced by normal cells

19
Q

TSA

A
  • proteins of genes not directly involved in forming the tumor
  • proteins of altered genes involved in transformation oncogenes; RAS, p53, chromosome translocation
20
Q

TAA

A
  • products of overexpressed genes
  • altered membrane glycolipid and glycoproteins
21
Q

tumor antigens

A

products of oncogenic viruses
viral peptides foreign > tumors immunogenic > CTLs
tumors more common with immunosupression

22
Q

Oncofoetal antigens

A
  • VERY high in normal foetus on tumor cells
  • de-repression on malignant transformation
  • released into serum
  • markers for diagnosis and following therapy
23
Q

Oncofetal antigen: carcinoembryonic Ag (CEA)

A
  • highly glycosylated, Ig superfamily member
  • intracellular adhesion molecule for tumor cells
  • high in colorectal carcinomas
24
Q

Oncofetal antigen: Alpha-foetoprotein (AFP)

A

from liver of foetus, high in liver cancer (also in germ cell tumors, liver cirrhosis)

25
Q

defects in antigen presentation

A
  • most healthy cells express MHC class I/ peptide complexes
  • in vitro studies show that tumor cells expressing tumor antiens by this mechansm fo on to be killed by CD8+ Tcells
  • tumor that has been selected not to express Class I / peptide have clear survival advantage
  • epithelial tumors, especially NSCLC have very poor class I expression
26
Q

what other defects are seen in antigen presenting

A
  • loss of functional b2 micro-globulin expression
  • loss of MHC class I alleles
27
Q

what are 3 down modulation molecules involved in antigen processing and presentation?

A
  • TAP 1/2
  • LMP 2/2
  • tapasin
28
Q

what does lack of co-stimulation cause?

A
  • melanoma cells are immunogenic but dont evoke antitumor immunity
  • lack of CD80/86 expression on cell surface which is required for costimulation of T cell alongside MHC binding
  • results in T cell biology and block in IL2 gene transcription
29
Q

what are immunosuppressive factors that are expressed/secreted by malignant cells or those surrounding cells within the stroma?

A
  • TGFb
  • VEGF
  • Prostaglandins
  • IL10 ; downregulates MHC class I
  • MCSF
  • tumor gangliosides ; suprress anti tumor responses
  • RCAS; inhibit prolif. induces apoptosis of T cells in vitro
29
Q

what are T-regulatory cells?

A
  • earlier known as T-suppressors
  • CD4+ Tcells with high expression of CD25 (a chain of IL-2 receptor)
30
Q

two types of T-regulatory cells

A
  • nTregs; Tregs developing in the thymus to ensure tolerance to self antigens
  • adaptable Tregs; naive CD4+ Tcells induced in the periphery
31
Q

how are T-regulatory cells identified?

A
  • by FOXP3; winged helical TF
  • vital for development and funciton of these cells as mutations lead to severe autoimmune condition
32
Q

what is the importance of Tregs?

A
  • found in far greater concs, in peripheral blood in patients with variety of cancers
  • found in far greater quantities within tumor milieu, ascites, draining lymph nodes in patients with cancer
33
Q

what is function of Treg?

A
  • mediate suppression on tumor specific CD4+ and CD8+ T cells via TCR
  • TGFb and IL10 thought to be secreted in vivo and membrane bound in TGFb also highly potent
  • research continues to reveal further modes by which Tregs mediate suppression
33
Q

targeting Tregs

A
  • anti CTLA-4; ipilimumab, tremelimumab
  • targeting CD25; LMB-2 fusion protein, Ontak
34
Q

targeting Tregs II

A
  • conventional chemotherapy drugs like cyclophosphamide in smaller more frequent dosing; depletes Tregs, enhances effector T cell function
  • Targeting GITR ; glucocorticoid induced tumor necrosis factor receptor ; against antibody DTA-1
35
Q

other immunoregulatory cells

A
  • myeloid derived suppressor cells; ROS and NO suppress T cell activity
  • NKT cells; produce IL10 and IL4 , Th2 directing
  • M2; Th2 directing APCs produce TGFb
  • chemokines; tumors produce CCL2, CCL17 and CCL22 recruit Tregs
36
Q

takeaway on immunosurveillance

A
  • immune system and tumor biology very closely intertwined
  • immune surveillance ongoing but imperfect
  • immunoediting critical in immune escape
  • multiple methods of immune evasion
37
Q
A

biology of cancer (13 decks)

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