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*
Section of Genetic Engineering, Research Center for Genetic Engineering and Cell Transplantation, and
Department of Immunology, Tokai University School of Medicine, Bohseidai, Isehara, Japan
A novel liver injury model was established in mice by
targeting of OVA-containing liposomes into the liver, followed by
adoptive transfer of OVA-specific Th1 cells. Combined treatment of mice
with OVA-containing liposomes and Th1 cell transfer caused an increase
in serum transaminase activity that was paralleled with an elevation of
serum IFN-
levels. In sharp contrast, OVA-specific Th2 cell transfer
resulted in an increase of serum IL-4 levels, but did not induce liver
injury. Neither NK, NK T, nor CD8+ T cells were required
for the Th1-induced liver injury. The liver injury was blocked by
anti-IFN- mAb and anti-TNF-
mAb, but not by anti-Fas
ligand mAb. The Fas/Fas ligand independency was also demonstrated using
Fas-deficient lpr mice. These findings indicate that Th1
cells are the major effector cells in acute liver
injury.
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