Immune surveillance hypothesis (Macfarlane Burnet, 1950s)
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1 TUMOR-IMMUNITÄT A.K. Abbas, A.H. Lichtman, S. Pillai (6th edition, 2007) Cellular and Molecular Immunology Saunders Elsevier Chapter 17, immunity to tumors
2 Immune surveillance hypothesis (Macfarlane Burnet, 1950s) importance still controversial but: it is clear that immune system reacts against tumor cells one of the factors in growth of malignant tumors: ability to evade or overcome mechanisms of host defense increased incidence of some tumor types in immunocompromized experimental animals and humans immune mechanisms can be exploited to destroy tumors
3 Expermental evidence: Methylcholantrene(MCA) -induced tumors
4 Tumor antigens: Tumor-specific: TSA Oncogenic mutants of normal cellular genes: ras, bcr-abl, p53 Randomly mutated genes: TSTA s (tumor-specific transplantation antigens) Can be identified: biochemical cdna cloning Tumor-associated: TAA Normal cellular proteins aberrantly expressed Tyrosinase - melanomas (enzyme melanin biosynthesis) Cancer/testis antigens: expressed testis and trophopblasts Oncofetal antigens: developing fetal tissue CEA: carcinoembryonic antigen - colon and many cancers, AFP: α-fetoptotein - hepatocellular cancer and others not specific, can be induced inflammatory conditions Altered glycolipid and glycoprotein antigens: gangliosides - in melanomas Mucin-1 - O-linked carbohydrates Tissue-specific differentiation antigens
5 Antigens of oncogenic viruses: DNA-viruses: EBV: Epstein-Barr HPV: papilloma Animals: Papovaviruses: SV40, polyoma Adenoviruses RNA viruses: Animal models In humans only HTLV-1 known: ATL, infects CD4+ cells
6 Tumor antigens recognized by T cells
7 Immune responses to tumors Innate: NK: MHC low, ligands for activating receptors (MICA, B, ULBP) LAK cells (IL2) Macrophages: direct by receptors? IFN-γ from T lymphocytes Adaptive: CD8+ cells: Clear for carcinogen-induced and virus-induced tumors Less clear for spontaneous But: tumor-specific CTL can be isolated from tumors Cross-presentation by professional APCs necessary to differentiate CD8+ cells to antitumor CTLs Use of pulsed DCs in tumor therapy CD4+ cells: not so clear Cytokines for CTL development TNF and IFN-γ - macrophage activation Antibodies: complement, Fc receptor (macrophages, NK) Little evidence for in vivo effective humoral response
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9 Evasion of immune responses: Induction of tolerance by TA: MMTV SV40T transgenic Anergy induction by presentation by APC inducing tolerance Regulatory T cells: found in tumors Loss of antigen expression MHC downregulation Failure to induce CTL: no costimulators or MHCII Products suppressing immune response: TGF-β Fas-L masking of cell surface: sialic acid containing mucopolysaccharides
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11 Immunotherapies Stimulation of active immune response Vaccination: Killed tumor vaccines + adjuvants Purified tumor antigens Pulsed DCs Cytokines and co-stimulator enhanced vaccines DNA vaccines Viral vectors: tumor antigens + cytokines Preventive versus therapeutic: hepatitis B HPV Augmentation by costimulators: B7 transfected tumor cells and cytokines: Il2, IL4, IFNs, GMCSF, TNF, IL12 Blocking inhibitory pathways: CTLA4 (autoimmunity!) Bacillus Calmette-Guerin Anti-CD3
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14 Passive immunotherapies: LAK: from PBLs, IL2 In mice impressive effects In patients wide individual variation TILs: from inflammatory infiltrate, trials ongoing Graft versus leukemia effect Anti-tumor antibodies - humanized Anti-CD30 Anti-HER2 Coupled to toxins: ricin, diphteria toxin Radioisotopes Anti-tumor drugs Anti-EGF: colorectal cancer Anti-VEGF: in combination with chemotherapeutic agents Anti-tumor antibodies used to clear tumor cells from bone marrow Before autologous BM transplantation
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17 Role of immune system in promoting tumor growth: Innate immune system: inflammation Macrophages (angiogenesis, tissue remodeling, free radicals/mutations) Gastric cancer by Heliobacter pylori Hepatocellular carcinoma by hepatitis B and C virus
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