Figure 7
Figure 7. IFN-α blockade promotes EC monolayer formation in SLE. Lupus PBMCs were cultured under proangiogenic conditions in the presence or absence of (A) blocking antihuman IFN-α mAb or isotype control or (B) antihuman type I IFN-R or isotype control (all 2 μg/mL). At day 15, anti–IFN-α– or anti–type I IFN-R–treated cells, but not controls, formed EC monolayers. Results are representative of independent experiments in SLE patients who failed to form EC monolayers, which corrected with anti–IFN-α (n = 9) or with anti–type I IFN-R (n = 6). (C) TLR7 and/or TLR9 blockade promotes EC monolayer formation in SLE. Lupus PBMCs were cultured in EGM20 supplemented with a control ODN, a TLR7 antagonist, a TLR9 antagonist, or a TLR7/9 antagonist (1 μM). Images were acquired after 15 days in culture. Results show cells from a representative SLE patient. All magnifications are × 20. See “In vitro differentiation into mature ECs” for more image acquisition information.

IFN-α blockade promotes EC monolayer formation in SLE. Lupus PBMCs were cultured under proangiogenic conditions in the presence or absence of (A) blocking antihuman IFN-α mAb or isotype control or (B) antihuman type I IFN-R or isotype control (all 2 μg/mL). At day 15, anti–IFN-α– or anti–type I IFN-R–treated cells, but not controls, formed EC monolayers. Results are representative of independent experiments in SLE patients who failed to form EC monolayers, which corrected with anti–IFN-α (n = 9) or with anti–type I IFN-R (n = 6). (C) TLR7 and/or TLR9 blockade promotes EC monolayer formation in SLE. Lupus PBMCs were cultured in EGM20 supplemented with a control ODN, a TLR7 antagonist, a TLR9 antagonist, or a TLR7/9 antagonist (1 μM). Images were acquired after 15 days in culture. Results show cells from a representative SLE patient. All magnifications are × 20. See “In vitro differentiation into mature ECs” for more image acquisition information.

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