The MHC class Ib molecule, CD1, has been conserved throughout mammalian evolution. To assess the function of CD1, we investigated the Concanavalin A induced hepatitis model that shows increased CD1 expression in hepatocytes. In this hepatitis model, NKT cells were found to be numerically expanded. Cytotoxicity of hepatic mononuclear cells (MNC) was activated by CD1 expression in the target cells and was strongly inhibited by CD1 transfectant used as cold targets. Furthermore, the hepatic MNC depleted of NKT cells demonstrated lower cytotoxic activity against GD1-expressing cells. These observations suggest the possibility that NKT cells recognize CD1 and have cytotoxic activity against CD1 expressing cells. In previous reports about the mouse hepatitis model, chemical factors such as IL 4 and TNF-α production from NKT cells were thought to be very important. Our study provides new insights into the mechanism through which direct interaction of CD1 and NKT cells takes place.
|ジャーナル||Sapporo Medical Journal|
|出版ステータス||Published - 01-12-1997|
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