Figure 5.
Figure 5. TNF-α-regulated expression of CD69 and CD137 after inhibition of the IKK2/NF-κB signaling pathway. Endothelial cells were infected with parental retrovirus or retrovirus containing dominant-negative IKK2 and subsequently stimulated with 2 ng/mL TNF-α for 16 hours. (A) Flow cytometry of CD69 surface expression revealed a significant induction by TNF-α in cells infected with the parental virus; this can be completely blocked in cells expressing dominant-negative IKK2. (B) In contrast to wild-type HUVECs, retrovirally infected HUVECs do not up-regulate CD137 upon exposure to TNF-α. Specific profiles are shown by thick lines and isotype control profiles appear as thin lines.

TNF-α-regulated expression of CD69 and CD137 after inhibition of the IKK2/NF-κB signaling pathway. Endothelial cells were infected with parental retrovirus or retrovirus containing dominant-negative IKK2 and subsequently stimulated with 2 ng/mL TNF-α for 16 hours. (A) Flow cytometry of CD69 surface expression revealed a significant induction by TNF-α in cells infected with the parental virus; this can be completely blocked in cells expressing dominant-negative IKK2. (B) In contrast to wild-type HUVECs, retrovirally infected HUVECs do not up-regulate CD137 upon exposure to TNF-α. Specific profiles are shown by thick lines and isotype control profiles appear as thin lines.

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