Immune Lecture 22 Study Notes.docx

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Microbiology and Immunology
Microbiology and Immunology 3300B

Immune Lecture 22 Study Notes 1. How can inflammation cause cancer? -many chronic inflammatory diseases increase the risk IBD = chronic inflammation of the GI tract can cause colon/rectal cancer (10% get it) within the general population, 0.05% develop colon or rectal cancer -reactive oxygen and nitrogen species can mutate DNA 2. What does ROS do? -can generate many mutated DNA bases -chemically altered forms of DNA created by superoxide or hydrogen peroxide -DNA repair might fix them but sometimes it doesn’t 3. Discuss inflammation, infection and cancer. -chronic infection can lead to cancer (helicobacter pylori = infection of the stomach) will colonize the stomach and induce inflammation this damage will lead to the cancer -some viruses carry cancer-causing genes oncovirus (enter infected cell and use gene to take over cell division) epstein-barr virus, kaposi’s sarcoma virus, HPV 4. How much of cancer do infections cause? -infections may cause up to 25% of all cancers -vaccination against these viruses can prevent these cancers 5. What is HPV? -human papilloma virus -causes cervical cancer (5 most common in women) -250 000 deaths per year 6. What are the different strains? -HPV-16, 18, 6 and 11 -6/11 mostly cause warts, rarely cancer -others cause cervical cancer -HPV can also cause anal, vaginal, penile, head, neck and oral cancers 7. Discuss the HPV vaccines. -guardacil protects against all forms -cervarix protects against 16 and 18 -both consist of empty (no genome) virus-like particles containing HPV organs 8. How well does the vaccine work? -farely new but so far in patients that have used it: majority are protected against precancerous lesions s 9. What helps tumours to grow? -inflammation 10.What purpose does tumor inflammation serve? -drives angiogenesis to provide blood supply to the growing tumor -creates a microenvironment which suppresses TH1 responses 11.Why is angiogenesis required for tumor growth? -cells need oxygen and nutrients to grow -when it stops growing the tumour will secrete VEGF which will cause new blood vessels to form, penetrate the tumour and allow more O2 and nutrients to expand -much larger and can metastasize 12.Why does tumor angiogenesis require immune cells? -neutrophils lie within the blood vessels -when they crawl out of them to go towards the tissue they create a channel -producing angiogenic factors/growth factors and create new endothetlial cells which will form the blood vessel -this gives the tumour a new blood vessel 13.How do we stop blood vessels from being formed? -experiment where Nu were killed using antibodies -if new channels aren’t formed then VEGF can’t be secreted to stimulate the growth of new blood vessels 14.What is a tumour associated macrophage? -somehow activates an M2 (alternatively) -they start producing anti inflammatory cytokines, pro-healing, angiogenic factors and neutrophil attractors -TFFbeta, IL-10, CXCL1/2/3/8, VEGF and VEGA 15.How do we get an M2? -monocytes enter the tumour are exposed to M-CSF, IL4/10/13 which turn it into an M2 -from here, it will produce CXCL1/2/3/8 which will recruit neutrophils in order to produce channels -VEGF/chemokines/cytokines produced to make angiogenesis occur -VEGF/VEGA also produced by macropage to stimulate angiogensis -M2 will release growth factors and tissue repair factors to stimulate tumour growth -M2 will release IL10 and TGFbeta -TGFbeta will cause T cells and DC to make TH2 or Treds while IL10 will stimulate more monocytes 16.Can inflammation kill cancer? -trying to tweak our immune system to be more tumor killing -kill tumour cells in high enough quantities: ROS, RNS, proteases, pore-forming proteins and antibody-dependent cell cytotoxicity 17.Can our adaptive immune system fight cancer? -experiments with mice: mice with certain immune mutations have a higher incidence of cancer gamma delta T-cells missing RAG/STAT1 (making T cells) knockouts perforin knockouts (released in granzymes) -experiment with mice: give them irradiated tumour cells (killed; so they c
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