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髓磷脂脂质在实验性变应性脑脊髓炎中的作用。III. 由髓磷脂碱性蛋白-半乳糖脑苷脂复合物诱导的实验性变应性脑脊髓炎恢复期豚鼠的抑制转移

The role of myelin lipids in experimental allergic encephalomyelitis. III. Transfer of suppression from guinea pigs recovering from EAE, induced by myelin basic protein--galactocerebroside complexes.

作者信息

Hosein Z Z, Gilbert J J, Strejan G H

出版信息

Cell Immunol. 1986 Apr 15;99(1):265-78. doi: 10.1016/0008-8749(86)90234-0.

DOI:10.1016/0008-8749(86)90234-0
PMID:2428529
Abstract

Juvenile strain 13 guinea pigs were immunized with myelin basic protein (MBP) combined with galactocerebrosides (MBP + GC) or with total myelin lipids without GC [MBP + (TL-GC)] in CFA. Control animals received dinitrophenylated-ovalbumin (DNP-OA) in CFA, CFA or IFA alone. The animals injected with MBP + GC showed a higher rate of recovery from the first EAE episode (83%) than those treated with MBP + (TL-GC) (50%). With the exception of the group treated with IFA alone, all animals were refractory to EAE following rechallenge with MBP in CFA 90 days after the first exposure. The in vitro proliferative response to MBP, of peripheral blood lymphocytes (PBLs) derived from guinea pigs freshly sensitized to MBP in CFA, was drastically suppressed in the presence of PBLs from animals injected with MBP + GC. Upon transfer to normal syngeneic recipients, spleen cells from MBP + GC-treated animals completely suppressed the clinical and histological manifestations of EAE following recipient challenge with MBP in CFA. Cell-free supernatants from PBLs and spleen cells of strain 13 guinea pigs treated with MBP + GC inhibited lymphocyte proliferation to MBP, of allogeneic responder cells, and spleen cell supernatants completely suppressed the induction of EAE upon transfer to allogeneic recipients. Suppression could not be transferred with cells from other treated groups. These results suggest that animals immunized with MBP + galactocerebrosides in CFA develop suppressor cells that may be in part responsible for the recovery from the first EAE episode and for protection against rechallenge with MBP in CFA. Their cell-free supernatants act in an MHC-nonrestricted fashion. These results do not rule out an additional protective mechanism since all animals exposed to CFA were refractory to rechallenge despite lack of demonstrable suppressor cell activity.

摘要

将幼年13号品系豚鼠用髓鞘碱性蛋白(MBP)与半乳糖脑苷脂(MBP + GC)联合或用不含GC的总髓鞘脂质[MBP + (TL - GC)]在完全弗氏佐剂(CFA)中进行免疫。对照动物在CFA中接受二硝基苯基化卵清蛋白(DNP - OA)、单独的CFA或不完全弗氏佐剂(IFA)。注射MBP + GC的动物从首次实验性自身免疫性脑脊髓炎(EAE)发作中恢复的比率(83%)高于用MBP + (TL - GC)处理的动物(50%)。除了单独用IFA处理的组外,所有动物在首次接触后90天用CFA中的MBP再次攻击时对EAE均具有抗性。在CFA中对MBP新鲜致敏的豚鼠外周血淋巴细胞(PBL)对MBP的体外增殖反应,在注射MBP + GC的动物的PBL存在下被显著抑制。将来自用MBP + GC处理的动物的脾细胞转移到正常同基因受体后,在用CFA中的MBP攻击受体后,完全抑制了EAE的临床和组织学表现。用MBP + GC处理的13号品系豚鼠的PBL和脾细胞的无细胞上清液抑制了同种异体反应细胞对MBP的淋巴细胞增殖,并且脾细胞上清液在转移到同种异体受体后完全抑制了EAE的诱导。抑制作用不能用来自其他处理组的细胞进行转移。这些结果表明,在CFA中用MBP +半乳糖脑苷脂免疫的动物产生了抑制细胞,这些抑制细胞可能部分负责从首次EAE发作中恢复以及防止在用CFA中的MBP再次攻击时发病。它们的无细胞上清液以MHC非限制性方式起作用。这些结果并不排除存在额外的保护机制,因为所有接触CFA的动物尽管缺乏可证明的抑制细胞活性,但对再次攻击均具有抗性。

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