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This metabolism-immunity crosstalk disrupts both innate and adaptive immunity: it drives the aberrant activation of macrophages and neutrophils while reprogramming T cell metabolismenhancing glycolysis in pro-inflammatory Th1/Th17 cells and impairing mitochondrial oxidative phosphorylation in Tregsultimately establishing a chronic intra-renal inflammatory microenvironment that accelerates glomerulosclerosis and tubulointerstitial fibrosis