Researchers have uncovered new insights into how tumor-derived lactate impairs the function of natural killer (NK) cells, a critical component of the immune system’s response to cancer. The study identifies lysine lactylation (Kla)—a posttranslational modification triggered by lactate—as a key factor in suppressing NK cell cytotoxicity within the tumor microenvironment.
NK cells are essential for recognizing and destroying cancerous cells, but their functionality often becomes diminished in tumor settings. One contributing factor is the high concentration of lactate, a metabolic by-product commonly elevated in tumors due to the Warburg effect, where cancer cells preferentially use glycolysis even under aerobic conditions.
The research demonstrates that lactate induces lysine lactylation in NK cells, interfering with their ability to carry out their cytotoxic role. Posttranslational modifications like Kla can alter protein function and cellular behavior, and in the case of NK cells, this modification leads to impaired immune surveillance.
By investigating the molecular pathways involved, scientists aim to develop strategies that augment NK cell resistance to lysine lactylation. Such approaches could preserve or even enhance NK cell efficacy within the hostile metabolic conditions of tumors, offering potential advancements in immunotherapy.
These findings provide a deeper understanding of NK cell suppression in cancer and open new avenues for therapeutic interventions designed to bolster the body’s innate ability to combat malignancies.
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