Fig 2: Detection of anti-APEX1 autoAb in sera of SLE patients using Western blotA. The presence of anti-APEX1 autoAb in SLE patients (n = 10) and NC (n = 10) detected using Western blot. Recombinant human APEX1 antigen was run on SDS-PAGE and transferred onto PVDF membrane. Sera from SLE or NC (1:500 dilution) were incubated with the strips of membrane for 2 h. After reaction with HRP-conjugated rabbit anti-human IgG, the strips were visualized by chemiluminescent substrate. The upper panel depicts the reaction of autoAb with APEX1 in sera of SLE and NC. The lower panel depicts the binding of the recombinant APEX1 antigen on the membrane with HRP-conjugated rabbit anti-APEX1 antibody as a loading and positive control. B. Relative quantity of the band intensities in SLE and NC samples (upper panel in A) and normalized to loading controls (lower panel in A).

Fig 3: Validation of the expression of 16 autoAbs using ELISA in a larger cohort of SLE and NCThe levels of 16 most differentially expressed autoAbs involved in apoptosis, cell cycle, and DNA repair pathways were measured using ELISA in a larger cohort of serum samples from SLE patients (n = 35) and NC (n = 30). Data were analyzed using GraphPad Prism 6.0 software with P values of Mann Whitney test presented in each plot. Differences with P < 0.05 are considered significant. Of the 16 autoAbs assayed, 12 autoAbs including those targeting APEX1, HMGB1, PADI4, IFIT5, POLB, VRK1, UBE2S, SRP19, AURKA, MAPKAPK3, AGO1, and RGS3, were identified as being increased significantly in SLE than in NC (P < 0.05).