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Figure 3 | Arthritis Research & Therapy

Figure 3

From: PDL241, a novel humanized monoclonal antibody, reveals CD319 as a therapeutic target for rheumatoid arthritis

Figure 3

PDL241 inhibits Ig production from PBMC by specifically depleting plasmablasts and plasma cells. (A) Time course of inhibition of IgM production from PBMC. Representative of n = 2 experiments. (B) Inhibition of IgM by PDL241 is dependent on mAb concentration and intact mAb, as F(ab’)2 fragments of PDL241 showed no activity. The dose dependent inhibition of IgM by PDL241 was demonstrated in >10 donors; F(ab’)2 experiment was a representative experiment of two. (C) Depletion of NK cells but not monocytes from PBMC reduces the inhibitory activity of PDL241. Representative experiment of n = 4; P = 0.01 for NK cell depleted compared to PBMC. (D) PDL241 treatment results in specific reduction in plasmablast counts in PBMC cultures. In contrast to rituximab (open bars), PDL241 treatment (closed bars) of PBMC specifically depleted plasma cells but not B cells from PBMC cultures. Counts were expressed as% of cIgG1-treated cultures. Data represent the mean and SD of n = 6 experiments from distinct donors. P ≤0.001 for B cell depletion by rituxan compared to PDL241 at 1 and 10 μg/ml. (E) CD319 was highly expressed on plasmablasts in PBMC cultures, (left panel, black histogram). Dot plots showing CD27 + CD38+ plasmablasts following treatment with cIgG1 control (middle panel) or PDL241 (right panel). Ig, immunoglobulin; mAB, monoclonal antibody; NK, natural killer; PBMC, peripheral blood mononuclear cells; SD, standard deviation.

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