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Significance SLC15A4 is a lysosome-resident amino acid/oligopeptide transporter that is preferentially expressed in immune cells. SLC15A4 is required for TLR7/9-dependent type I interferon production and plays a critical role in the pathogenesis of lupus and colitis. However, the precise molecular mechanisms of SLC15A4-mediated inflammatory responses are still undetermined. We revealed that SLC15A4 loss disturbed the coupling of glycolysis and the TCA cycle, and SLC15A4-deficient macrophages preferred to use glutamine rather than glucose as a carbon source for the TCA cycle. SLC15A4-deficient macrophages produced low levels of itaconate and proinflammatory IL-12 cytokine members. Our results reveal a mechanism of metabolic regulation in which an amino acid transporter acts as a guardian to allow macrophages to acquire an M1-prone metabolic phenotype.

SLC15A4 mediates M1-prone metabolic shifts in macrophages and guards immune cells from metabolic stress