Metabolic regulation of the immune cell in psoriasis: mechanisms and interventions

Abstract

Psoriasis is increasingly recognized as a metabolically regulated inflammatory skin disease. Aberrant glycolysis, oxidative phosphorylation, lipid metabolism, and amino acid metabolism reshape T cell, dendritic cell, macrophage, and neutrophil responses, driving chronic inflammation. Keratinocyte-derived metabolites further amplify immune dysfunction, establishing a reciprocal metabolic–immune circuit. Targeting immunometabolic checkpoints, including glucose transporter transporters, mammalian target of rapamycin signaling, and amino acid transporters, offers promising strategies to modulate pathogenic immune responses. This review highlights the metabolic reprogramming of key immune subsets in psoriasis and outlines future directions for developing selective metabolic interventions to improve therapeutic outcomes in this disease context.