Targeting glutamine metabolism to enhance CAR-macrophage efficacy in solid tumors

A recent study has demonstrated the power of metabolic engineering in enhancing the antitumor activity of chimeric antigen receptor (CAR) macrophages (CAR-Ms) in solid tumors. By overexpressing the glutamine transporter SLC38A2, researchers successfully reprogrammed the glutamine utilization pathway in CAR-Ms, significantly improving their anti-tumor activity against HER2-positive breast cancer cells. This metabolic reprogramming enhanced macrophage effector functions, including phagocytosis and cytokine production, thus boosting the overall immune response within the tumor microenvironment (TME). These findings suggest that integrating metabolic strategies with immunotherapy can provide a new avenue for improving CAR-M-based treatments in solid tumors.