Abstract
Abstract Due to its lethality, fulminant hepatitis, the most severe form of viral infection in liver, is a global health concern. Here we examine the function of Th17 cells during the mouse hepatitis virus (MHV) induced hepatitis. We find that IL17 levels in serum are rapidly upregulated and positively correlated to liver damage and death of mice upon viral infection. The unresponsiveness of host cells to IFNγ significantly enhances virus-induced Th17 response. Unrestricted IL17 production accounts for severe liver damage as well as detrimental inflammation in infected IFNγ receptor deficient (IFNγR-/-) mice, since neutralization of IL17 effectively suppresses inflammation and protects mice from liver injury. IFNγ facilitates antigen-induced apoptosis of Th17 cells in vitro and adoptive transfer of IFNγR deficient, but not IFNγR competent CD4+ T cells leads to enhanced liver damage in wild-type mice. The results demonstrate an essential role of Th17 cells in MHV-induced immunopathology and indicate the importance of IFNγ in maintaining immune balance between Th1 and Th17 responses during the acute viral infection.
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