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Natural killer cell activation contributes to hepatitis B viral control in a mouse model.

Abstract：

:The roles of CD4 + T cells and CD8 + T cells in hepatitis B virus (HBV) infection have been well documented. However, the role of innate immunity in HBV infection remains obscure. Here we examined the effect of activation of innate immunity by polyinosinic: polycytidylic acid (PolyI:C) on HBV infection. A chronic HBV replication mouse model was established by hydrodynamical injection of pAAV/HBV1.2 plasmid into C57BL/6 mice. We found that HBV did not seem to induce an active NK-cell response in the mouse model. Early PolyI:C treatment markedly decreased serum HBV levels and led to HBV clearance. Following PolyI:C injection, NK cells were activated and accumulated in the liver. Depletion of NK cells markedly attenuated the anti-HBV activity of PolyI:C. Moreover, we found that IFN-γ production from NK cells was essential for the antiviral effect of PolyI:C in the model. Importantly, activation of NK cells by PolyI:C could also lead to HBV suppression in HBV-tolerant mice and HBV-transgenic mice. These results suggest that activated NK cells might suppress HBV and contribute to HBV clearance during natural HBV infection. In addition, therapeutic activation of NK cells may represent a new strategy for the treatment of chronic HBV infection.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Tong S,Liu G,Li M,Li X,Liu Q,Peng H,Li S,Ren H,Yin W

doi

10.1038/s41598-017-00387-2

subject

Has Abstract

pub_date

2017-03-22 00:00:00

pages

314

issue

1

issn

2045-2322

pii

10.1038/s41598-017-00387-2

journal_volume

7

pub_type

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