Intracellular interleukin-32γ mediates antiviral activity of cytokines against hepatitis B virus.

Abstract:

:Cytokines are involved in early host defense against pathogen infections. In particular, tumor necrosis factor (TNF) and interferon-gamma (IFN-γ) have critical functions in non-cytopathic elimination of hepatitis B virus (HBV) in hepatocytes. However, the molecular mechanisms and mediator molecules are largely unknown. Here we show that interleukin-32 (IL-32) is induced by TNF and IFN-γ in hepatocytes, and inhibits the replication of HBV by acting intracellularly to suppress HBV transcription and replication. The gamma isoform of IL-32 (IL-32γ) inhibits viral enhancer activities by downregulating liver-enriched transcription factors. Our data are validated in both an in vivo HBV mouse model and primary human hepatocytes. This study thus suggests that IL-32γ functions as intracellular effector in hepatocytes for suppressing HBV replication to implicate a possible mechanism of non-cytopathic viral clearance.

journal_name

Nat Commun

journal_title

Nature communications

authors

Kim DH,Park ES,Lee AR,Park S,Park YK,Ahn SH,Kang HS,Won JH,Ha YN,Jae B,Kim DS,Chung WC,Song MJ,Kim KH,Park SH,Kim SH,Kim KH

doi

10.1038/s41467-018-05782-5

subject

Has Abstract

pub_date

2018-08-16 00:00:00

pages

3284

issue

1

issn

2041-1723

pii

10.1038/s41467-018-05782-5

journal_volume

9

pub_type

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