In exploring an aspect of how killer T cells generate the raw materials required for their proliferation, a study has uncovered an unexpected link between the immune cells' metabolism, regulation of gene expression, persistence and functional efficacy that could be exploited using existing drugs to improve cancer immunotherapy.
In exploring an aspect of how killer T cells generate the raw materials required for their proliferation, a Ludwig Cancer Research study has uncovered an unexpected link between the immune cells' metabolism, regulation of gene expression, persistence and functional efficacy that could be exploited using existing drugs to improve cancer immunotherapy.
"We show in this study that CD8+ T cells indeed engage this metabolic pathway, and that an extensively characterized metabolic enzyme known as isocitrate dehydrogenase plays a central role in the process," said Ho."But what really surprised us -- and could be significant for cancer immunotherapy -- is that genetically or pharmacologically disrupting the enzyme did not hamper the proliferation or function of CD8+ T cells, as we expected it would.
Analysis of how disrupting IDH2 activity affected the T cells revealed a link between an altered profile of metabolites in them and epigenetic regulation of their gene expression, in which the chemical tagging of DNA and its protein packaging dynamically alters chromosome structure to determine the availability of genes for reading.
Specifically, IDH2 inhibition affects a core metabolic process known as the TCA cycle, forcing the T cells to activate compensatory metabolic pathways. This alters the profile of metabolites in the cells, boosting the levels of molecules that inhibit an epigenetic enzyme known as KDM5 and so changing the deposition of a key epigenetic"mark" on their chromosomes.
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Disrupting a core metabolic process in T cells may improve their therapeutic efficacyIn exploring an aspect of how killer T cells generate the raw materials required for their proliferation, a Ludwig Cancer Research study has uncovered an unexpected link between the immune cells' metabolism, regulation of gene expression, persistence and functional efficacy that could be exploited using existing drugs to improve cancer immunotherapy.
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