Knospe W H, Steinberg D, Gratwohl A, Speck B
Int J Cell Cloning. 1984 Jul;2(4):263-71. doi: 10.1002/stem.5530020406.
Immunologically mediated aplastic anemia (AA) in mice was induced by the i.v. injection of 10(7) lymph node cells (LNC) from H-2k identical but Mls mismatched CBA/J donor mice into previously irradiated (600 rad total body gamma) C3H/HeJ mice. Cyclosporin A (CsA), 25 mg/kg, was administered subcutaneously from day -1 to day 30. Control mice included C3H/HeJ mice which received 600 rad alone, C3H/HeJ mice which received 600 rad plus CsA as above, and C3H/HeJ mice which received 600 rad total body irradiation followed by 10(7) LNC from CBA/J donors. CsA failed to prevent lethal AA. These results suggest that the pathogenetic mechanisms operating in immunologically mediated AA differ from the mechanisms operating in rodents transplanted with allogeneically mismatched marrow or spleen cells which develop graft-versus-host disease. The results are consistent with a non-T cell-dependent mechanism causing the AA.
通过静脉注射来自H-2k相同但Mls不匹配的CBA/J供体小鼠的10⁷个淋巴结细胞(LNC)到先前接受过照射(全身γ射线600拉德)的C3H/HeJ小鼠中,诱导小鼠发生免疫介导的再生障碍性贫血(AA)。从第-1天到第30天,皮下给予25mg/kg的环孢素A(CsA)。对照小鼠包括仅接受600拉德照射的C3H/HeJ小鼠、接受600拉德照射加上述CsA的C3H/HeJ小鼠,以及接受全身600拉德照射后再注射来自CBA/J供体的10⁷个LNC的C3H/HeJ小鼠。CsA未能预防致死性AA。这些结果表明,免疫介导的AA的发病机制与移植了发生移植物抗宿主病的异基因不匹配骨髓或脾细胞的啮齿动物的发病机制不同。结果与一种非T细胞依赖性机制导致AA一致。