Strejan G H, St Louis J
Department of Microbiology and Immunology, University of Western Ontario, London, Canada.
Cell Immunol. 1990 May;127(2):284-98. doi: 10.1016/0008-8749(90)90133-c.
In previous experiments, we showed that administration of myelin basic protein (MBP) inserted into phosphatidyl-serine liposomes, to susceptible animals suppressed the clinical manifestations of both acute and chronic-relapsing EAE. In this report we compare the effectiveness of treatment with MBP-liposomes and with MBP-coupled syngeneic spleen cells in EAE protection. Lewis rats treated with 150 micrograms MBP-liposomes or with 160 micrograms (35 x 10(6] MBP-coupled spleen cells, given 7 days before and 7 days after encephalitogenic challenge were equally protected against clinical EAE, when compared to untreated controls. In addition to clinical protection, in vitro proliferative responses of lymphocytes from treated rats were significantly reduced, but delayed hypersensitivity (DTH) reactions remained unaffected. Proliferation of lymphocytes from MBP-sensitized donors was inhibited by the addition of spleen cells but not of lymph node cells from treated donors. The inhibitory effect was observed with spleen cells regardless of whether the donors were treated or not, was antigen nonspecific, and localized in a radio-resistant, adherent cell population. Adoptive transfers of spleen cells from treated donors, after a 48-hr in vitro incubation with concanavalin A, showed that the cells from donors treated with MBP-coupled spleen cells, but not with MBP-liposomes, suppressed the disease in recipients, following challenge with MBP-complete Freund's adjuvant (CFA). These results suggest that two distinct mechanisms operate in the protection by MBP-coupled cells and MBP-liposomes, respectively.
在先前的实验中，我们发现，将插入磷脂酰丝氨酸脂质体的髓鞘碱性蛋白（MBP）给予易感动物，可抑制急性和慢性复发性实验性自身免疫性脑脊髓炎（EAE）的临床表现。在本报告中，我们比较了用MBP-脂质体和MBP偶联的同基因脾细胞治疗在EAE保护中的效果。与未治疗的对照组相比，在致脑炎攻击前7天和攻击后7天给予150微克MBP-脂质体或160微克（35×10⁶）MBP偶联脾细胞治疗的Lewis大鼠，对临床EAE具有同等的保护作用。除了临床保护外，治疗大鼠淋巴细胞的体外增殖反应显著降低，但迟发型超敏反应（DTH）未受影响。添加来自治疗供体的脾细胞而非淋巴结细胞可抑制MBP致敏供体淋巴细胞的增殖。无论供体是否接受治疗，脾细胞均具有抑制作用，该作用是非抗原特异性的，且定位于抗辐射的黏附细胞群体。用伴刀豆球蛋白A体外孵育48小时后，将来自治疗供体的脾细胞进行过继转移，结果显示，用MBP偶联脾细胞而非MBP-脂质体治疗的供体的细胞，在接受MBP-完全弗氏佐剂（CFA）攻击后，可抑制受体中的疾病。这些结果表明，MBP偶联细胞和MBP-脂质体的保护作用分别通过两种不同机制发挥作用。
