Identification of autoantibody clusters that best predict lupus disease activity using glomerular proteome arrays
J. Clin. Invest. Quan Li Zhen, et al. 115:3428 doi:10.1172/JCI23587 [Go to this article.]

Figure 4
DNA dependence of glomerular-reactive autoantibodies in lupus. For all the B6 and B6.Sle1.lpr mouse sera studied (total, n = 27; A and B), the reactivity to DNA/chromatin was compared to the reactivities to total glomerular lysate or Matrigel, within the same serum samples. Shown are the scatter plots (and correlation coefficients) relating mouse IgG reactivities against chromatin versus Matrigel (A) and mouse IgM reactivity against dsDNA versus glomerular extract (B). (C and D) Mean remnant IgG (C) and IgM (D) seroreactivities to dsDNA or to the different glomerular Ags following DNAse-I pretreatment of the glomerular proteome array slides, the test sera alone, or both, expressed as a percentage of the fluorescence intensities recorded in sham-treated controls, arbitrarily set at 100%. Each bar represents the mean value derived from 3 individual B6.Sle1.lpr serum samples that had expressed high reactivity to the depicted glomerular targets. All IgG seroreactivities remaining after both the sera and the Ag arrays were DNAse-I treated (C) were significantly less than the sham-treated controls (P < 0.05 for fibrinogen IV; P < 0.01 for myosin; and P < 0.001 for all the other Ags), with the exception of α-actinin (P > 0.05). Likewise, all IgM seroreactivities remaining after both the sera and the Ag arrays were DNAse-I treated (D) were significantly less than the sham-treated controls (P < 0.01 for aggrecan and P < 0.001 for the other Ags), with the exceptions of fibrinogen IV and α-actinin (P > 0.05).