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HDAC6 Mediates Poly (I:C)-Induced TBK1 and Akt Phosphorylation in Macrophages

Yan Wang1,2, Ke Wang1, Jian Fu2

  • 1Department of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.

Frontiers in Immunology
|August 28, 2020
PubMed

Insights

Histone deacetylase 6 (HDAC6) suppresses antiviral immunity in macrophages. Deleting HDAC6 enhances interferon-beta production and reduces suppressor cytokine IL-10, boosting innate antiviral defense.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Macrophages are crucial for innate antiviral immunity, producing cytokines like interferons (IFNs) and IL-10.
  • Type I IFNs activate antiviral defenses, while IL-10 suppresses them.
  • HDAC6, a tubulin deacetylase, influences cell signaling pathways.

Purpose of the Study:

  • To investigate the role of HDAC6 in macrophage antiviral responses.
  • To examine HDAC6's effect on poly (I:C)-induced IFN-β and IL-10 production.
  • To analyze HDAC6's impact on key antiviral signaling pathways (TBK1, GSK-3β, Akt).

Main Methods:

  • Utilized mouse bone marrow-derived macrophages (BMDMs) stimulated with poly (I:C).
  • Assessed IFN-β and IL-10 cytokine production.
  • Investigated the activation status of signaling molecules TBK1, GSK-3β, and Akt in wild-type and HDAC6-deleted BMDMs.

Main Results:

  • HDAC6 deletion enhanced poly (I:C)-induced IFN-β production by up-regulating TBK1 activity and reducing GSK-3β inhibition.
  • HDAC6 deletion inhibited poly (I:C)-induced IL-10 production, linked to suppressed Akt activation.
  • HDAC6 negatively regulates macrophage antiviral responses.

Conclusions:

  • HDAC6 modulates macrophage production of IFN-β and IL-10 via TBK1, GSK-3β, and Akt signaling pathways.
  • HDAC6 acts as a suppressor of the innate antiviral immune response in macrophages.
  • Targeting HDAC6 may represent a strategy to enhance antiviral immunity.
Keywords:
acetylationcytokineinfectioninnate immunitymicrotubule

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