Fig. 4

Upregulated genes in PBMC of SLE were significantly enriched in the interferon signaling pathway. a A diagram showing the interferon signaling pathway and upregulated genes involved in the network. b Array-based mRNA expression represented by normalized intensity in SLE LN⁺, SLE LN⁻, and normal controls.^*Indicates p < 0.05 as compared to normal controls. c Interferon scores for SLE patients and controls. The IFN score for each sample was derived from the combined fold change of relative intensity for each gene. The mean intensity in normal controls for each gene was calculated and used as baseline intensity for the gene. Then the intensity of mRNA expression for each gene in patients or controls was normalized with the baseline intensity and resulted in the fold change of relative intensity. The interferon score was a sum of relative intensity for the nine genes (shown in Fig. 5b) that were significantly enriched in the interferon pathway. d Hierarchical clustering of the differentially methylated CpG sites on the upregulated genes associated with the interferon signaling pathway. Hypomethylated CpG sites were identified in all the upregulated IFN genes. e The CpG sites in MX1, IFIT1 and IFIT3 genes were hypomethylated in SLE patients comparing with NC. ^*Indicates p < 0.05. f The mRNA expression of IFN genes (IFT1, IFT3 and MX1) were reversely correlated with the methylation status of the CpG sites in PBMC. NC normal controls, SLE systemic lupus erythematosus, SLE LN ⁺ SLE with lupus nephritis, SLE LN ⁻ SLE without lupus nephritis