Figure 4
Figure 4. Increased IFN-α expression in lupus EPCs/CACs. (A) Lupus serum prevents monolayer formation by healthy control EPCs/CACs. Control PBMCs were plated on fibronectin-coated wells with complete EC media in the presence or absence of 20% allogeneic control or SLE sera. At day 15, EC monolayer formation was assessed. Images are representative of 7 of 8 SLE serum samples and 4 of 4 control serum samples used in 5 allogeneic control PBMCs. Images represent bright field (top), diI–ac-LDL (middle), and UEA-1–FITC (bottom) of allogeneic control cells exposed to 1 representative SLE serum sample (left) and 1 representative control serum sample (right; × 10 objective magnification). See “In vitro differentiation into mature ECs” for more image acquisition information. (B) Graphs represent percentage IFN-α expression (± SEM) of 13 SLE and 6 controls in PBMCs cultured under proangiogenic conditions. (C) IFN-α expression on day 1–cultured cells of a representative control and SLE patient. (D) EPC/CAC supernatants and autologous serum from SLE patients induce higher expression of IFN-α–inducible genes in epithelial cell lines than controls. Results represent fold induction of IFN-inducible genes (mRNA) and are presented as mean (± SEM) of supernatants or sera from 8 controls and 23 SLE patients. Data are normalized to HPRT-1.

Increased IFN-α expression in lupus EPCs/CACs. (A) Lupus serum prevents monolayer formation by healthy control EPCs/CACs. Control PBMCs were plated on fibronectin-coated wells with complete EC media in the presence or absence of 20% allogeneic control or SLE sera. At day 15, EC monolayer formation was assessed. Images are representative of 7 of 8 SLE serum samples and 4 of 4 control serum samples used in 5 allogeneic control PBMCs. Images represent bright field (top), diI–ac-LDL (middle), and UEA-1–FITC (bottom) of allogeneic control cells exposed to 1 representative SLE serum sample (left) and 1 representative control serum sample (right; × 10 objective magnification). See “In vitro differentiation into mature ECs” for more image acquisition information. (B) Graphs represent percentage IFN-α expression (± SEM) of 13 SLE and 6 controls in PBMCs cultured under proangiogenic conditions. (C) IFN-α expression on day 1–cultured cells of a representative control and SLE patient. (D) EPC/CAC supernatants and autologous serum from SLE patients induce higher expression of IFN-α–inducible genes in epithelial cell lines than controls. Results represent fold induction of IFN-inducible genes (mRNA) and are presented as mean (± SEM) of supernatants or sera from 8 controls and 23 SLE patients. Data are normalized to HPRT-1.

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