Cancer immunology and immunotherapy
7 important questions on Cancer immunology and immunotherapy
In which 2 stages can immunotherapy interfere?
- Priming and activation (anti-CTLA4)
- killing of cancer cells (anti-PDL1)
How can blocking CTLA4 be an option for immunotherapy?
How can antibodies against PD1 (or its ligand) be used as immunotherapy?
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How can immune-related adverse events (like toxicity) originate?
By which mechanisms can adverse effects (like skin problems, ocular, liver, bone barrow, neuropathies) be caused?
- Increasing T-cell activity against antigens that are present in tumors and healthy tissue (e.g heart)
- increasing levels of pre-existing autoantibodies
- increasing level of inflammatory cytoskines (e.g intestine)
- enhancing complement-mediated inflammation due to direct binding of an anti-CTLA4 antibody with CTLA4 expressed on normal tissue (e.g brain)
Via which 4 strategies can vaccines work on the immune system by cancer antigen presentation?
- Tumor cells (antologous/allogenic)
- tumor antigens (peptides, proteins, RNA, DNA)
- antigen-presenting cells (antigen-loaded DCs)
- effector cells (autologous T-cells, genetically engineered T-cells)
How are DC (dendritic cell) vaccines created?
To check such vaccines, there is looked at immunologic responses upon DC vaccination, safety/feasibility, progression-free survival, overall survival and QOL (quality of life).
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