LIVER-INJURY MODEL IN MICE INDUCED BY A CELLULAR IMMUNOLOGICAL MECHANISM - DELAYED-TYPE HYPERSENSITIVITY-INDUCED LIVER-INJURY TO PICRYL CHLORIDE AND PHENOTYPE OF EFFECTOR CELL

Liver injury was induced in BALB/c mice by local delayed-type hypersen sitivity (DTH) to picryl chloride (PC1). Distinct changes of biochemic al parameters were observed including the elevation of serum alanine a nd aspartate aminotransferases, increase of liver lipid peroxides, as well as decrease of serum alkaline phosphatase. Damage was confirmed b y histopathological findings such as hepatocellular necrosis, granuloc yte infiltration, and fatty degeneration. The liver injury was passive ly transferred into naive syngeneic mice by infusing spleen cells from immune mice. The capacity of the splenocytes to induce liver injury i n recipient mice was almost completely abolished by pretreatment of th e cells with anti-Thy 1.2 or anti-CD4, but not anti-CDS antibody. Thes e findings suggest that the production of liver injury by a local DTH mechanism is possible and the subpopulation of T cells, Thy-1.2(+), L3 T4(+), and Lyt-2(-) cells, is at least one of the effector cells that mediate the injury. (C) 1996 Academic Press, Inc.