Methylation of immune synapse genes modulates tumor immunogenicity.
basic_science · Level V
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- Record sourced from PubMed, PMID 31714899.
- Also identified by DOI 10.1172/JCI131234 and PMC identifier 6994116.
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Abstract
Cancer immune evasion is achieved through multiple layers of immune tolerance mechanisms including immune editing, recruitment of tolerogenic immune cells, and secretion of immunosuppressive cytokines. Recent success with immune checkpoint inhibitors in cancer immunotherapy suggests a dysfunctional immune synapse as a pivotal tolerogenic mechanism. Tumor cells express immune synapse proteins to suppress the immune system, which is often modulated by epigenetic mechanisms. When the methylation status of key immune synapse genes was interrogated, we observed disproportionately hypermethylated costimulatory genes and hypomethylation of immune checkpoint genes, which were negatively associated with functional T cell recruitment to the tumor microenvironment. Therefore, the methylation status of immune synapse genes reflects tumor immunogenicity and correlates with survival.
Medical subject headings
- DNA Methylation
- DNA, Neoplasm
- Epigenesis, Genetic
- Gene Expression Regulation, Neoplastic
- Genes, Neoplasm
- Immunological Synapses
- Neoplasms
- Tumor Microenvironment