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Studies on protective immunity against malaria

疟疾保护性免疫研究

基本信息

批准号：
62570171
负责人：
WAKI Seiji
金额：
$ 1.09万
依托单位：
Gunma University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

1. Mechanisms of acquisition of protective immunity against malaria was investigated by comparative studies on infections with virulent plasmodium berghei (Pb NK65) and its attenuated derivative (Pb XAT) in mice. In Pb NK65 infection, mice showed suppressive response in antibody production and delayed-type hypersensitivity and development of auto antibodies against lymphocytes. Mice infected with Pb XAT did not show these responses but developed solid protective immunity against Pb NK65 infection accompanied with high antibody titer. When such an immune serum was transferred into mice Pb XAT infection was eliminated completely. These results showed that Pb XAT stimulates antibody production which contributes protection against the parasites. On the contrary, in Pb NK65 infection harmful immunopathological responses against host are more prominent than protective immune responses against the parasites. 2. Role of T cells in two aspect of immunity to Pb was examined in mice by administration of monoclonal antibodies (MAB) against T cell subsets or lymphokines. First, mice treated with anti Lyt. 2 mAb showed significantly longer survival from infection with Pb NK65 compared with intact or anti L3T4 mAb administration. This phenomenon was also observed in mice by treatment with anti gamma-IFN mAb. second, in Pb XAT infection, administration with either anti L3T4 or anti gamma-IFN mAb precluded induction of protective immunity. These findings reveal that CD4^+ T cells might be responsible for protection and CD8^+ T cells for immunopathology of the infected hosts and gamma-IFN must be effector molecules in both immune responses.

1.通过对伯氏疟原虫强毒株（Pb NK 65）及其减毒衍生物（Pb XAT）感染小鼠的比较研究，探讨了小鼠获得抗疟保护性免疫的机制。在铅NK 65感染，小鼠表现出抑制反应的抗体产生和迟发型超敏反应和发展的自身抗体的淋巴细胞。感染Pb XAT的小鼠没有表现出这些反应，但对Pb NK 65感染产生了高抗体滴度的保护性免疫。将该免疫血清转移到小鼠体内后，PbXAT感染被完全消除.这些结果表明，铅XAT刺激抗体的产生，这有助于保护免受寄生虫。相反，在Pb NK 65感染中，对宿主的有害免疫病理反应比对寄生虫的保护性免疫反应更突出。2.本文用抗T细胞亚群单克隆抗体（MAB）和抗淋巴因子单克隆抗体（MAB）研究了T细胞在小鼠铅免疫中的两个方面的作用。首先，用抗Lyt治疗的小鼠。与完整或抗L3 T4 mAb给药相比，2 mAb显示Pb NK 65感染的存活时间显著延长。在用抗γ-IFN mAb处理的小鼠中也观察到这种现象。第二，在Pb XAT感染中，施用抗L3 T4或抗γ-IFN mAb排除了保护性免疫的诱导。这些发现表明，CD 4 ^+ T细胞可能负责保护，CD 8 ^+ T细胞可能负责感染宿主的免疫病理学，γ-IFN在这两种免疫应答中一定是效应分子。