Smith C I, Cooksley W G, Powell L W
Clin Exp Immunol. 1980 Mar;39(3):618-25.
The possible pathogenetic role of lymphocytes sensitized to liver antigens was investigated in CBA mice in which sublethal hepatic necrosis had been induced by carbon tetrachloride (CCl4). Sensitized lymphocytes from CCl4-treated mice were administered to syngeneic recipients. The recipients developed sensitivity to liver antigens but showed no evidence of liver damage. The cell mediating the immune response both in the donor and the recipient was a T cell. This was demonstrated further by studies involving mice rendered T cell deficient. These mice did not develop sensitized lymphocytes when they were treated with CCl4 but the extent of liver damage was similar in both T cell-depleted and intact animals. These findings suggest that T cell sensitization to liver antigens occurs as a result of toxic liver damage and does not play a role in the pathogenesis of the hepatic necrosis.
在通过四氯化碳(CCl4)诱导了亚致死性肝坏死的CBA小鼠中,研究了对肝脏抗原致敏的淋巴细胞可能的致病作用。将来自CCl4处理小鼠的致敏淋巴细胞给予同基因受体。受体对肝脏抗原产生了敏感性,但未显示出肝损伤的迹象。在供体和受体中介导免疫反应的细胞是T细胞。涉及使T细胞缺陷的小鼠的研究进一步证明了这一点。这些小鼠在用CCl4处理时未产生致敏淋巴细胞,但在T细胞耗竭和完整的动物中肝损伤程度相似。这些发现表明,对肝脏抗原的T细胞致敏是毒性肝损伤的结果,在肝坏死的发病机制中不起作用。