Silberman S L, Jacobs R P, Cole G A
Infect Immun. 1978 Feb;19(2):533-9. doi: 10.1128/iai.19.2.533-539.1978.
Sublethal irradiation (500 R) of C3H mice is followed by a gradual replacement of radiosensitive cells in their spleens by surviving stem cells originating in bone marrow. This compensatory hemopoiesis was quantitated by counting the numbers of stem cell-derived colonies appearing on spleen surfaces, as well as those which grew in vitro after marrow cells, suspended in soft agar, were overlaid onto syngenic mouse embryo fibroblast feeder layers. Compensatory colony formation, both in vivo and in vitro, was severely depressed when mice were infected with lymphocytic choriomeningitis virus (LCMV) 1 day before irradiation, although the induction of virus-specific cytotoxic T cells in their spleens was unimpaired. Without irradiation, mice, acutely infected with LCMV, showed a dramatic reduction in the numbers of specific antibody-forming cells generated in their spleens after priming with sheep erythrocytes during week 1 post-infection, yet the ability of their marrow cells to form colonies in vitro remained normal. Therefore, the basis of immunodepression is distinct from that of defective hemopoiesis since the latter is apparent only when LCMV infection is accompanied by irradiation. However, as discussed, both phenomena may be related to alterations induced within the splenic environment by LCMV.
对C3H小鼠进行亚致死剂量照射(500伦琴)后,其脾脏中对辐射敏感的细胞会逐渐被源自骨髓的存活干细胞所取代。通过计数出现在脾脏表面的干细胞衍生集落数量,以及将悬浮于软琼脂中的骨髓细胞接种到同基因小鼠胚胎成纤维细胞饲养层上后在体外生长的集落数量,对这种代偿性造血进行了定量分析。当小鼠在照射前1天感染淋巴细胞性脉络丛脑膜炎病毒(LCMV)时,体内和体外的代偿性集落形成均受到严重抑制,尽管其脾脏中病毒特异性细胞毒性T细胞的诱导未受损害。在未进行照射的情况下,急性感染LCMV的小鼠在感染后第1周用绵羊红细胞致敏后,其脾脏中产生的特异性抗体形成细胞数量显著减少,但其骨髓细胞在体外形成集落的能力仍保持正常。因此,免疫抑制的基础与造血缺陷的基础不同,因为后者仅在LCMV感染伴有照射时才明显。然而,如前所述,这两种现象可能都与LCMV在脾脏环境中诱导的改变有关。