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. 2016 Jan 8;35(4):429–442. doi: 10.15252/embj.201592586

Figure 2. HDAC6 positively regulates the innate antiviral response in bone marrow‐derived macrophages and peripheral blood mononuclear cells.

Figure 2

  • A, B
    Virus replication at 12 and 24 hpi, in HDAC6 +/+ and HDAC6 −/− BMDMs in response to VSV‐GFP (MOI = 10) infection (A) and PR8‐GFP (MOI = 5) infection (B).
  • C
    Virus replication in HDAC6 +/+ and HDAC6 −/− BMDMs in response to HSV‐GFP (MOI = 2) infection.
  • D
    Virus replication in HDAC6 +/+ and HDAC6 −/− PBMCs in response to VSV‐GFP (MOI = 10) infection.
  • E
    ELISA of IFN‐β (upper), IL‐6 (lower) levels in the supernatant of (A) and (B), and in HDAC6 +/+ and HDAC6 −/− BMDMs treated with poly(I:C) (20 μg/ml) or transfected with 5′ppp‐dsRNA (1 μg/ml).
  • F
    Immunoblot analysis of the phosphorylated and inactive forms of IRF3, IKBα, TBK1, RIG‐I, MAVS, HDAC6, and β‐actin at the indicated times (0, 2, 4, 8, and 16 h) in HDAC6 +/+ and HDAC6 −/− BMDMs. BMDMs were stimulated with PR8‐GFP (MOI = 3).
  • G
    Induction of mRNA for type I IFN, IL‐6, and other IFN‐related antiviral genes in HDAC6 +/+ and HDAC6 −/− BMDMs in response to a RIG‐I agonist stimulation at 6 h. HDAC6 +/+ and HDAC6 −/− BMDMs were stimulated with 5′ppp‐dsRNA (0.5 μg/ml) for 6 h.
Data information: Data are representative of at least two independent experiments. Error bars, mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 (Student's t‐test).Source data are available online for this figure.