Hoffsten P E, Villalobos R, Hill C, Klahr S
Kidney Int. 1977 May;11(5):318-26. doi: 10.1038/ki.1977.49.
Mice chronically infected with the virus of lymphocytic choriomeningitis (LCM) develop immune complex glomerulonephritis. Others have shown that adoptive immunization of these mice by the i.p. injection of syngeneic immune spleen cells terminates the chronic viral carrier state. The present studies were designed to define the effector cell from the immune spleen responsible for adoptive immunization and to determine the effect of this procedure upon the immune complex nephritis which occurs in LCM carrier mice. The results indicate that the effector cell in adoptive immunization is a T-cell that functions directly as a killer cell when transferred to LCM carrier mice. Sixteen of nineteen adoptively immunized mice examined had less immune complex material deposited in their glomeruli than control unmanipulated litter mates. These data demonstrate that this animal model of immune complex glomerulonephritis is immunodeficient with respect to LCM virus-specific killer T-cells. Transfer of this cell population to the LCM carrier mouse diminishes the animal's viremia and improves its immune complex nephritis. In view of these observations, it is suggested that the rationale for the use of immunosuppressive therapy in spontaneously occurring glomerulonephritis should be carefully reconsidered.
长期感染淋巴细胞性脉络丛脑膜炎（LCM）病毒的小鼠会患上免疫复合物肾小球肾炎。其他人已经表明，通过腹腔注射同基因免疫脾细胞对这些小鼠进行过继免疫可以终止慢性病毒携带状态。本研究旨在确定负责过继免疫的免疫脾中的效应细胞，并确定该程序对LCM携带小鼠中发生的免疫复合物肾炎的影响。结果表明，过继免疫中的效应细胞是一种T细胞，当转移到LCM携带小鼠中时，它直接作为杀伤细胞发挥作用。在检查的19只过继免疫小鼠中，有16只肾小球中沉积的免疫复合物物质比未处理的对照同窝小鼠少。这些数据表明，这种免疫复合物肾小球肾炎的动物模型在LCM病毒特异性杀伤性T细胞方面存在免疫缺陷。将这群细胞转移到LCM携带小鼠中可减少动物的病毒血症并改善其免疫复合物肾炎。鉴于这些观察结果，建议应仔细重新考虑在自发性肾小球肾炎中使用免疫抑制疗法的基本原理。
