Figure 5
Both TNF-α induced ISG expression and antiviral activity against HCV and HEV were abrogated by its inhibitor Humira.
(A) In the Huh7 cell-based NF-κ B luciferase reporter cells, the TNF-α inhibitor, Humira, abrogated TNF-α induced NF-κ B-related luciferase activation as measured at 3 different time points (n = 3 independent experiments with 2–3 replicates each). (B) Same as (A) for the Huh7 cell-based ISRE luciferase reporter cells. (C) In Huh7 cells, the TNF-α inhibitor, Humira, abrogated TNF-α induced ISG expression as measured by qRT-PCR (n = 4). (D) In the Huh7 cell-based subgenomic HCV replicon, Humira abrogated the TNF-α induced anti-HCV effect as measured at 3 different time points (n = 3 independent experiments with 2–3 replicates each). (E) Same as (D) for Huh7 cell-based subgenomic HEV replicon. (F) TNF-α levels in serum samples collected from anti-TNF-α treatment naive Crohn’s disease patients were measured by ELISA kit (left). Serum samples with higher TNF-α levels showed stronger ISRE-related luciferase activity compared with control serum as measured at 3 different time points. Data presented as mean ± SD. (*P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant).
