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* Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, and Departments of
Parasitology and
Ophthalmology, Graduate School of Medical Sciences; Kyushu University, Fukuoka, Japan;
PRESTO, Japan Science and Technology Agency, Saitama, Japan;
¶ Ontario Cancer Institute and Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario, Canada; and
|| Department of Biomolecular Sciences, Faculty of Medicine, Saga University, Saga, Japan
Administration of Con A induces liver injury that is considered to be an experimental model for human autoimmune or viral hepatitis, where immunopathology plays roles mediated by activated lymphocytes, especially NK1.1+ CD3+ NKT cells, and inflammatory cytokines, including IFN-
and IL-4. In the present study we investigated the role of WSX-1, a component of IL-27R, in Con A-induced hepatitis by taking advantage of WSX-1 knockout mice. WSX-1-deficient mice were more susceptible to Con A treatment than wild-type mice, showing serum alanine aminotransferase elevation and massive necrosis in the liver. Although the development of NKT cells appeared normal in WSX-1 knockout mice, purified NKT cells from the knockout mice produced more IFN- and IL-4 than those from wild-type mice in response to stimulation with Con A both in vitro and in vivo. In addition, hyperproduction of proinflammatory cytokines, including IL-1, IL-6, and TNF-
, was observed in the knockout mice after Con A administration. These data revealed a novel role for WSX-1 as an inhibitory regulator of cytokine production and inflammation in Con A-induced hepatitis.
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