Figure 5
Figure 5. IFN-α treatment prevents EC monolayer formation in healthy controls. (A) Control PBMCs were plated on fibronectin-coated wells with complete EC media in the presence or absence of graded concentrations of recombinant IFN-α. At day 15, EC monolayer formation was assessed. Images are from experiments from 4 representative controls. Similar results were seen in 4 SLE patients using similar concentrations of IFN-α. Magnifications are × 10. See “In vitro differentiation into mature ECs” for more image acquisition information. (B-E) IFN-α induces CAC apoptosis and skewing toward other myeloid cell subsets. Representative dot plots display percentage apoptotic CD14+ CACs in untreated and IFN-α–treated cells. Graphs represent mean (± SEM) percentage expression of myeloid subsets on the EC monolayer of 5 controls after IFN-α treatment. * indicates P < .05.

IFN-α treatment prevents EC monolayer formation in healthy controls. (A) Control PBMCs were plated on fibronectin-coated wells with complete EC media in the presence or absence of graded concentrations of recombinant IFN-α. At day 15, EC monolayer formation was assessed. Images are from experiments from 4 representative controls. Similar results were seen in 4 SLE patients using similar concentrations of IFN-α. Magnifications are × 10. See “In vitro differentiation into mature ECs” for more image acquisition information. (B-E) IFN-α induces CAC apoptosis and skewing toward other myeloid cell subsets. Representative dot plots display percentage apoptotic CD14+ CACs in untreated and IFN-α–treated cells. Graphs represent mean (± SEM) percentage expression of myeloid subsets on the EC monolayer of 5 controls after IFN-α treatment. * indicates P < .05.

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