Cutting edge: Inhibition of hepatitis B virus replication by activated NK T cells does not require inflammatory cell

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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
07:25

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Published on: September 25, 2019

K Kakimi1, T E Lane, F V Chisari

  • 1Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 12, 2001
PubMed

Insights

Activated NK T cells in the liver can inhibit hepatitis B virus replication. This antiviral effect is achieved through direct cytokine production by NK T cells, not by recruiting other inflammatory cells.

Area of Science:

  • Immunology
  • Hepatology
  • Virology

Background:

  • Intrahepatic Natural Killer T (NK T) cells activated by alpha-galactosylceramide noncytopathically inhibit hepatitis B virus (HBV) replication in mouse models.
  • This inhibition is attributed to antiviral cytokines produced by activated NK T cells or recruited inflammatory cells.

Purpose of the Study:

  • To investigate the specific mechanisms by which activated NK T cells control HBV replication within the liver.
  • To determine the role of cytokine-induced chemokine production and inflammatory cell recruitment in the antiviral activity of NK T cells.

Main Methods:

  • Utilized a transgenic mouse model of hepatitis B virus replication.
  • Administered alpha-galactosylceramide to activate intrahepatic NK T cells.
  • Measured the production of interferon-gamma (IFN-gamma) and CXC chemokine ligands 9 and 10 (CXCL9, CXCL10).
  • Assessed the recruitment of lymphomononuclear inflammatory cells into the liver.

Main Results:

  • Activated NK T cells produced IFN-gamma.
  • IFN-gamma induced liver parenchymal and nonparenchymal cells to produce CXCL9 and CXCL10.
  • These chemokines mediated the intrahepatic recruitment of lymphomononuclear inflammatory cells.
  • Viral replication was controlled even without the recruitment of these inflammatory cells.

Conclusions:

  • Direct activation of intrahepatic NK T cells is sufficient to control HBV replication in this model.
  • The antiviral effect is primarily mediated by cytokines produced directly by NK T cells, independent of inflammatory cell recruitment.
  • IFN-gamma plays a role in chemokine-mediated inflammatory cell trafficking, but this is not essential for the direct antiviral activity.

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