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Cancer, Immunity and Immunotherapy

4 important questions on Cancer, Immunity and Immunotherapy

What is an immune escape by tumor cells?

1. Tumour cells increase MIC expression
2. NKG2D on NK and γδ T cells binds MIC, killing tumour cells (MIC = MHC class I chain related molecules)
3. Variant tumour cells shed soluble MIC, which binds lymphocyte NKG2D --> so they can't kill the tumor cells
4. Variant tumour cells survive and proliferate

What are two forms of immunotherapies in cancer that use antibodies? But why do these not work for everyone?

- Checkpoint blockade: anti-PD1/PDL1 antibodies: this allows T cell killing of tumour cell  T cell only gets activating signal not inhibiting signal that tumour cells give to T cells
- Checkpoint blockade: anti-CTLA4 antibodies: blocks co-stimulation to inactivate the T cell and thus activates the T cells
--> However, due to the many muatations that form through the replication these antibodies can stop working

How can specific T cell responses be measured in cancer?

Analysing the neo-antigen-specific T cell response in cancer:
i. Generate map of tumour-specific mutations (ExomeSeq)
ii. Determine which mutated genes are expressed (RNASeq)
iii. Predict epitopes for each mutation/each HLA-allele in silico
iv. Screen for T cell recognition of mutated epitopes

How does DC based vaccination work against cancer?

- Monocytes isolated from a prostate cancer patient are cultured with a fusion protein of GM-SCF and prostatic acid phosphatase (PAP)
- GM-CSF induces the monocytes to mature into dendritic cells. PAP is internalized with the GM-CSF and is processed into peptides that are presented by MHC class II
- The activated DC are fused into the patient, where they travel to the spleen and present PAP antigens to naïve T cells

The question on the page originate from the summary of the following study material:

Immunobiology

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