Immunology and Immune Disorders - cancer and the immune system
- Created by: Rosa
- Created on: 30-03-13 20:01
cancer cells ignore apoptosis cues and make their own proliferation cues
HMPCC hereditary nonpolyposis corectal cancer - insides of GI tract covered in small tumours - family history
6 seperate mutations to develope cancer?
exetrinsic factors:
- tobacco smoke
- pollution
- radiation
- chemicals
- viruses - Hep b and EBV
heamotological malignancies - 8% leukemia and lymophoma
sarcoma - 2% osteosarcoma
carcinoma - 80% breast lung colon
MAGE 1 - silent toumour antigen: germline cell in testes (normal), if found anywhere else it is indicativeof tomour
immune surveillance - cytotoxic t-lymphocytes
spontaneous solid tumours:
- mutation causes protein to be potentially recognised and non-self by CTL's
- naive t cells circulate in blood, lympoh and secondary organs
- tumour cells lack co-stimulatory molecules,
- no circulation so cannot prevent
heamatological malignancies:
- found where t-cells circulate
- heam malignancies express high levels of B7 providing co-stimulation (not 100% fool proof)
Virus associated tumours:
- viruses causing acute infections do not cause cancer, cells are quickly destroyed
- viruses that cause cancer cause long term latent infections, so CTL's are no tgood
role of macrophages and NK cells
Hyperactivated macrophages express TNF (tumour necrosis factor) which causes tumour cell necrosis
Abnormal expression of surface molecules eg phosphatidylserine enables macrophages to differentiate between cancer and normal cells
NK (natural killer) cells target cells with low MHC (major histocompatibility complex) class I expression and display unusual surface molecules
Advantages-macrophage and NK are quick acting, recognize diverse targets, macrophages located in tissues where 92% tumours arise
Disadvantage-both macrophages and NK cells are reliant on inflammatory reaction
Genomic instability keeps tumour cells one step ahead of CTL surveillance
Tumour antigen mutate so no longer recognized
Tumour antigen mutate so no longer fit into MHC groove for presentation
Lack MHC expression (15% of all tumours)
Mutations of TAP transporters prevent tumour antigens being transported to MHC molecules
Genomic instability keeps tumour cells one step ahead of CTL surveillance
Tumour antigen mutate so no longer recognized
Tumour antigen mutate so no longer…
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