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 [
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Figure 6Five distinct clusters of IgG autoreactivity in lupus sera. (
A–
E) The autoantigen seroreactivities that apparently clustered together in Figure
5 were reassessed for correlation in a pairwise fashion. Indicated within each matrix are the corresponding correlation coefficients when seroreactivity to the different Ags were compared for concordance. For array Ags not listed in
A, the seroreactivity correlation coefficients between any 2 Ags were
r < 0.2, with the exception of concordance between SS-A/SS-B and Sm/RNP seroreactivity. (
F–
J) Seroreactivity levels noted in lupus sera (
n = 37) against the 5 clusters of targeted Ags, parsed according to their total SLEDAI scores. When available, glomerular pathology class was indicated (red, grade IV GN; green, grade II/III GN; blue, grade V GN; white, no biopsy done). (
F) For cluster 1 Ags, reactivity to laminin is plotted as the cluster’s representative. (
G) For cluster 2 Ags, reactivity to total histone is plotted as the cluster’s representative. (
H) For cluster 3 Ags, reactivity to dsDNA is plotted as the cluster’s representative. (
I) For cluster 4 Ags, reactivity to chondroitin sulphate is plotted as the cluster’s representative. (
J) For cluster 5 Ags, reactivity to fibrinogen IV is plotted as the cluster’s representative. The dotted line within each plot pertains to the cutoff for normality, representing mean ± 2 SD noted in the 11 normal control sera studied. (
K) Scatter-plotted serum concentrations of complement C3 (
y axis) versus IgG anti-dsDNA Ab levels (representative of cluster 3 seroreactivity;
x axis).