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. 2015 Mar 11;7(4):464–476. doi: 10.15252/emmm.201404719

Figure 1. Anti-BDCA2 mAb inhibits IFNα production by pDCs and induces internalization of BDCA2 on the surface of pDCs.

Figure 1

  • A, B Whole blood or PBMC were treated with increasing concentrations of 24F4A and stimulated with CpG-A for 16 h at 37°C. Anti-BDCA2-mediated IFNα inhibition in whole-blood assays (A). IFNα levels were detected using human IFNα ELISA. Graph depicts average of duplicate wells of one representative donor (n = 10). IC50 of 24F4A-mediated IFNα inhibition (B) in whole blood (circles) (n = 10) and PBMC (n = 18) from healthy human donors (squares) or SLE patients (triangles) (n = 11). Horizontal bar represents the mean IC50 for each sample type. Error bars represent SD of IC50 between donors.
  • C Anti-BDCA2-mediated internalization in whole-blood assays. Whole blood was treated with increasing concentrations of 24F4A for 16 h. Mean fluorescence intensity (MFI) of BDCA2 was determined with a non-cross-blocking anti-BDCA2 mAb (2D6). Shown is a representative plot of 10 experiments conducted.
  • D The IC50 of 24F4A-mediated IFNα inhibition was compared to the EC50 of 24F4A-induced BDCA2 internalization.
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