Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis
J. Clin. Invest. Haidong Dong, et al. 111:363 doi:10.1172/JCI16015 [
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Figure 2Preferential expression of B7-H1 mAb on activated CD4
+ T cells. (
a) On the left, 293 cells were transfected with mock (pcDNA3 vector) or human B7-H1 plasmid (pcDNA3-B7-H1cDNA) for 48 hours. B7-H1/293 cells were pretreated with 20 μg of control Ig (mIgG1) or 5H1 before staining with PD-1Ig (5 μg). On the right, activated M99 CTL cells were pretreated with 10 μg of mIgG1 or 5H1 before staining with B7-H1Ig (10 μg). B7-H1 mAb, PD-1Ig, or B7-H1Ig were used to stain the transfected 293 cells and activated M99 CTL cells. Representative fluorescence histograms of isotype control reagents (open lines) and B7-H1 mAb or fusion proteins (filled lines) are shown. (
b) Induction of B7-H1 expression on human T cell subsets. Human PBMCs were activated with PHA for indicated times and subjected to FACS analysis with B7-H1 mAb and mAb to CD4, CD8, or CD45RO. The numbers indicate the percentage of B7-H1 and CD4, CD8, or CD45RO double-positive cells in total populations, and the percentage in parentheses indicates the percentage of B7-H1–positive cells in each CD4
+, CD8
+, or CD45RO
+ subsets.