Journal
JOURNAL OF IMMUNOLOGY
Volume 167, Issue 12, Pages 6701-6705Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.12.6701
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Funding
- NCI NIH HHS [CA40489] Funding Source: Medline
- NIAID NIH HHS [AI40696] Funding Source: Medline
- NINDS NIH HHS [NS37336] Funding Source: Medline
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We have previously reported that intrahepatic NK T cells activated by alpha -galactosylceramide inhibit hepatitis B virus replication noncytopathically in the liver of transgenic mice. This effect is mediated by antiviral cytokines directly produced by activated NK T cells and/or by other cytokine-producing inflammatory cells that are recruited into the liver. In this study, we demonstrated that IFN-gamma produced by activated NK T cells induced parenchymal and nonparenchymal cells of the liver to produce high levels of CXC chemokine ligands 9 and 10, which mediated the intrahepatic recruitment of lymphomononuclear inflammatory cells. Recruitment of these cells was not necessary for the antiviral activity, indicating that direct activation of the intrahepatic resident NK T cell is sufficient to control viral replication in this model.
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