Fig 1: Inhibition of IC-induced glycolytic switch reduces autoantibody-mediated renal inflammation in vivo. (A) Ighg1 expression in whole kidney tissue from NZB/W kidneys versus controls. Means are indicated. Data derived from GEO: GSE27045. (B) Correlation of Il1b with Ighg1 mRNA levels in renal tissue from NZB/W mice shown in A. (C) qPCR of Hk2, Hif1a, and Il1b mRNA in renal tissue of MRL/MpJ and MRL-lpr mice and MRL/MpJ mice injected with Ova-IC. Data are normalized to gene expression in MRL/MpJ mice and Hprt. Means are indicated. (D) Correlation of glycolysis-associated genes and Il1b mRNA in renal tissue pooled from MRL/MpJ and MRL-lpr mice. (E) Serum urea levels in mice 24 h after i.v. injection of nephrotoxic serum (anti-GBM) with or without pretreatment with 2DG (n = 6 to 7 per group). Medians are indicated. (F) Representative kidney confocal images of mice treated as in E. (G) Quantification of neutrophils in kidneys of mice treated as in G (n = 4 to 10 per group). Medians indicated. (H) qPCR of human kidney cells stimulated with Ova-IC ± 2DG for 12 h. Data are normalized to Ova control and HPRT1. (I) Graphical summary of IgG IC-induced metabolic reprogramming in kidney macrophages. For in vivo experiments (C–G), medians are indicated, and each point represents a single kidney. For human kidney stimulations, means ± SEM are indicated from triplicate measurements. Data are representative of two or three independent experiment. P values were calculated using limma with multiple comparisons correction using the BH procedure (A), linear regression analysis (B), nonparametric Mann–Whitney U test (C, E, and G), or the two-tailed Student t test (H; *P < 0.05; **P < 0.01; ***P < 0.0001; ****P < 0.0001).