Abstract
Tumors with an inflamed tumor microenvironment are considered “hot tumors” and show good responses to immune checkpoint inhibitors (ICIs). Conversely, non-inflamed tumors, so-called “cold tumors,” have no tumor-suppressive cytokines and rarely respond to ICIs. Therefore, turning non-inflamed (cold) tumors into inflamed (hot) tumors is important for maximizing the effect of ICIs. We showed that lactate, a product of the Warburg effect, inhibited the efficacy of ICIs and suppressed IL-12 p40 expression in dendritic cells (DCs) through reducing NF-κB p65, p50 and c-Rel DNA-binding activity to the IL-12 p40 promoter.
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