权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Analysis of a common mechanism for the induction of cell-mediated immunity by intracellular bacteria and its application to host defense against bacterial infection.

分析细胞内细菌诱导细胞介导免疫的常见机制及其在宿主防御细菌感染中的应用。

基本信息

批准号：
02454176
负责人：
MITSUYAMA Masao
金额：
$ 4.03万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1992
项目状态：
已结题

项目摘要

This study was carried out to analyze the common mechanisms involved in the induction of cell-mediated immunity to intracellular bacteria including Listeria and Mycobacteria, and the following results were obtained. (1)The ineffectiveness of killed bacterial cells in the induction of specific immunity is not attributable to the amount of antigen or to the peristence of bacterial antigen in mice. (2)T cells generated in mice after immunization with viable bacteria could be activated by both viable and killed bacterial cells and the presence of HSP is not responsible for the induction of protective T cells. (3)Among various strains of L.monocy- togenes, some strains were found to be ineffective for the induction of specific immunity even if used as viable bacterial vaccine. The ability to induce protective immunity was correlated with the ability of each strain to induce macrophage production of IL-1. (4)Administration of recombinant IL-1 along with immunization with killed bacteria significantly promoted the development of antigen-specific T cells in mice. (5)The IL-1-inducing ability of Listeria was attributable to the production of 58KDa-hemolysin, listeriolysin O. (6)Production of IFN-gamma was indispensable for the expression of protective immunity by antigen- specific CD4 T cells and those which produce cytokine other than IFN-gamma could not afford the protective immunity.These results indicated that monokine production including IL-1 is critically required in the induction of cell-mediated immunity to intracellular bacteria and that IFN-gamma-producing ability is indispensable for the final expression of protective immunity by antigen-specific CD4^+ T cells.

本研究对李斯特菌和分枝杆菌等胞内细菌诱导细胞免疫的一般机制进行了分析，获得了以下结果。(1)灭活的细菌细胞在诱导特异性免疫方面的无效不是由于抗原量的多少或细菌抗原在小鼠体内的滞留。(2)活菌免疫小鼠后产生的T细胞可被活菌和灭活菌激活，热休克蛋白的存在不参与保护性T细胞的诱导。(3)在各种菌株中，有一些菌株即使作为活的细菌疫苗也不能有效地诱导特异性免疫。诱导保护性免疫的能力与每个菌株诱导巨噬细胞产生IL-1的能力相关。(4)重组IL-1联合灭活菌免疫可显著促进小鼠抗原特异性T细胞的发育。(5)李斯特氏菌的IL-1诱导能力与其产生58 KDa溶血素、李斯特溶血素O有关。(6)产生干扰素-γ是抗原特异性CD4T细胞表达保护性免疫所必需的，而产生干扰素-γ以外的细胞因子则不能提供保护性免疫。