Allan J E, Doherty P C
Cell Immunol. 1985 Feb;90(2):401-7. doi: 10.1016/0008-8749(85)90204-7.
Adoptively transferred immune spleen cells induce fatal neurological disease in cyclophosphamide-suppressed recipients injected intracerebrally (ic) with a large, but not small, dose of neurotropic lymphocytic choriomeningitis (LCM) virus. The elimination of virus from brain in the latter group, which survives without developing symptoms, depends upon the presence of Lyt 2+ lymphocytes. However removal of Lyt 2+ subset which is cytotoxic in vitro does not diminish the severity of the inflammatory process in vivo, though the onset of clinical disease is delayed in mice given Lyt 2-depleted populations and a larger ic dose of virus. The present findings are consistent with the idea that fatal LCM results from acute, synchronous damage to key functional cells in the central nervous system by virus-immune Lyt 2+, lymphocytes. Even so, if the number of virus-infected CNS cells is still relatively small at the time of T cell invasion, neurological symptoms are not recognized and the mice survive.
过继转移的免疫脾细胞，在经环磷酰胺处理、脑内注射大剂量（而非小剂量）嗜神经性淋巴细胞性脉络丛脑膜炎（LCM）病毒的受体中，会诱发致命的神经系统疾病。后一组受体在未出现症状的情况下存活，其脑中病毒的清除依赖于Lyt 2⁺淋巴细胞的存在。然而，体外具有细胞毒性的Lyt 2⁺亚群的去除，并不会减轻体内炎症过程的严重程度，尽管给予Lyt 2⁺细胞耗竭群体和更大脑内病毒剂量的小鼠临床疾病的发作会延迟。目前的研究结果与以下观点一致，即致命的LCM是由病毒免疫的Lyt 2⁺淋巴细胞对中枢神经系统关键功能细胞的急性、同步损伤所致。即便如此，如果在T细胞侵入时，病毒感染的中枢神经系统细胞数量仍然相对较少，就不会出现神经症状，小鼠也能存活。
