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. 2020 Aug 9;12(4):261–278. doi: 10.1007/s13238-020-00751-5

Figure 1.

Figure 1

HDAC3 positively regulates type I interferon production. (A) Luciferase activity in shNC, shHDAC3-1 or shHDAC3-2 cell lines (1 × 105), transfected for 36 h with a luciferase reporter for IFN-β (IFN-β-luc) or for ISRE (ISRE-luc), uninfected or infected with SeV for 10 h before luciferase assays were performed. HDAC3-Knockdown efficiency in the shHDAC3 cell lines were confirmed by immunoblotting analysis (lower). (B) ELISA analysis of IFN-β in the supernatant of shNC, shHDAC3-1 cell lines, followed by infection with or without SeV, VSV, HSV-1. (C) ELISA of IFN-β in the supernatant of THP-1 HDAC3-deficient cells (HDAC3 KO-1, HDAC3 KO-2), followed by infection with different stimulus (as shown). HDAC3 knockout efficiency in the THP-1 cells were confirmed by immunoblotting analysis (right). (D) Luciferase activity assay in HEK293T cells (1 × 105), co-transfected for 36 h with empty vectors, increased amounts of HDAC3 expression plasmids or Flag tagged HDAC3-H134Q (100 ng) together with a luciferase reporter for IFN-β (IFN-β-luc) or for ISRE (ISRE-luc), followed by infection with or without SeV for 10 h before luciferase assays were performed. (E) ELISA analysis of IFN-β in the supernatant of HEK293T cells (1 × 105), transfected for 36 h with empty vectors, increased amounts of HDAC3 expression plasmids or Flag tagged HDAC3-H134Q (100 ng), followed by infection with or without SeV for 10 h. (F) ELISA of IFN-β analysis in the supernatant of HDAC3-stable-expressing THP-1 cells, followed by infection with different stimulus (as shown). Data are representative of three independent experiments. Graphs show mean ± SD; n = 3. *P < 0.05; ** P < 0.01; ***P < 0.001 (Student’s t-test)