Liver injury was induced in BALB/c mice by local delayed-type hypersensitivity (DTH) to picryl chloride (PC1). Distinct changes of biochemical parameters were observed including the elevation of serum alanine and aspartate aminotransferases, increase of liver lipid peroxides, as well as decrease of serum alkaline phosphatase. Damage was confirmed by histopathological findings such as hepatocellular necrosis, granulocyte infiltration, and fatty degeneration. The liver injury was passively transferred into naive syngeneic mice by infusing spleen cells from immune mice. The capacity of the splenocytes to induce liver injury in recipient mice was almost completely abolished by pretreatment of the cells with anti-Thy 1.2 or anti-CD4, but not anti-CD8 antibody. These findings suggest that the production of liver injury by a local DTH mechanism is possible and the subpopulation of T cells, Thy-1.2+, L3T4+, and Lyt-2- cells, is at least one of the effector cells that mediate the injury.
|Number of pages||6|
|State||Published - Jan 10 1996|
Bibliographical noteFunding Information:
1Project supported by the National Natural Science Foundation of China, No. 39270784, and by the Foundation of State Educational Committee of China for Young Researcher, No. (1992)551. 2To whom correspondence should be addressed.
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