Doherty P C, Allan J E
Cell Immunol. 1987 Jun;107(1):1-7. doi: 10.1016/0008-8749(87)90259-0.
The induction of severe inflammatory process and fatal neurological disease by transfer of lymphocytic choriomeningitis virus (LCMV)-immune T cells into cyclophosphamide (Cy)-suppressed LCMV-infected mice is greatly inhibited by treatment of these recipients with antibody to the asialo GM1 ganglioside (anti-ASGM1). Examination of cytotoxic activity in lymphoid tissue of the Cy-suppressed recipients at 72 hr after cell transfer revealed that anti-ASGM1 treatment prevented the development of the cytotoxic T lymphocyte (CTL) response, even though the dose of antibody used did not significantly decrease CTL generation in unsuppressed mice. Abrogation of CTL activity was also observed following antibody treatment of NK-deficient (bg/bg) Cy-suppressed recipients, indicating that the anti-ASGM1 was unlikely to be operating via removal of NK cells that are in some way involved in the development of the CTL response. The possibility that anti-ASGM1 may act directly on T cells should be considered in all protocols involving the use of this reagent in immunosuppressed mice.
将淋巴细胞性脉络丛脑膜炎病毒（LCMV）免疫的T细胞转移到经环磷酰胺（Cy）抑制的LCMV感染小鼠体内会引发严重的炎症过程和致命的神经疾病，而用抗唾液酸GM1神经节苷脂抗体（抗ASGM1）治疗这些受体可极大地抑制这一过程。在细胞转移后72小时检测经Cy抑制的受体淋巴组织中的细胞毒性活性，结果显示抗ASGM1治疗可阻止细胞毒性T淋巴细胞（CTL）反应的发生，尽管所用抗体剂量并未显著降低未受抑制小鼠体内CTL的生成。在用抗体治疗NK缺陷（bg/bg）的经Cy抑制的受体后也观察到CTL活性的消除，这表明抗ASGM1不太可能通过清除以某种方式参与CTL反应发生的NK细胞来发挥作用。在所有涉及在免疫抑制小鼠中使用该试剂的实验方案中，都应考虑抗ASGM1可能直接作用于T细胞的可能性。
