ROLE OF CD4-CELLS IN REGULATING THE CHRONIC DEVELOPMENT OF LIVER-INJURY INDUCED BY DELAYED-TYPE HYPERSENSITIVITY TO PICRYL CHLORIDE( AND CD8+ T)

In this study we first investigated the cellular immune responses in m ice with chronic liver injury induced by delayed-type hypersensitivity to picryl chloride (PCI). A continuous reduction, after week 3 of liv er injury, was observed in the level of PCl-induced contact sensitivit y but not in sheep red blood cell-induced footpad reaction, suggesting the presence of PCl-specific suppression. When spleen cells from mice whose liver had been injured for 1 week were systemically transferred into syngeneic recipients with the liver injury, the elevation in ser um lactic dehydrogenase and the decrease in alkaline phosphatase and a lbumin levels in recipient mice were significantly exacerbated. Howeve r, when the liver damage in the donor mouse was allowed to proceed for 3, 5 or 7 weeks, biochemical changes in recipients were reduced to ne ar normal levels. A flow-cytometric assay demonstrated that the number of CD4+ T cells in both spleen cells and liver nonparenchymal cells d ecreased dramatically during the late phase of liver injury, while CD8 + counts did not. These findings suggest that CD4+ and CD8+ T lymphocy tes may contribute to the positive and negative regulation, respective ly, of the early and late phases in the chronic development of liver i njury.