Prevention of SLE-like syndrome by NAPc2 treatment. (A) Anti-CL titers in MRL-lpr mice treated with 0.5 mg/kg NAPc2 every second day starting at an age of 11 weeks; n = 6, P ≤ .0007; 2-way ANOVA, Sidak multiple comparisons test. (B) Anti-CL and β2GPI titers in an independent cohort with the same randomization and treatment scheme; n = 6, P ≤ .0001; 2-way ANOVA, Sidak multiple comparisons test. (C) Lymphadenopathy score for NAPc2- or saline-treated MRL-lpr mice; n = 6 per group, ∗P ≤ .05; 2-way ANOVA, Sidak multiple comparisons test. (D) Heatmap of the top 500 most significantly differentially expressed genes in splenic DCs from MRL-lpr mice isolated at the end of the treatment experiment; counts are z-scale normalized. Gene set enrichment analysis (GSEA) confirmed that NAPc2 suppresses inflammatory responses in DCs sorted from spleen; P-adjust threshold <.05 was used in GSEA (n = 4 per group). (E) Renal pathology scores and glomerular immune cell infiltration of NAPc2- or saline-treated MRL-lpr mice; n = 12 mice per group, ∗P < .025; Mann-Whitney U test. Scale bars, 50 mm. (F) Albuminuria in NAPc2- or saline-treated MRL-lpr mice determined at the end of the experiment. Combined data from the cohorts shown in panels A and B; P = .0768, unpaired t test with Welch correction.