Analysis for the pathogenesis of concomitant infection in AIDS and murine AIDS
Analysis for the pathogenesis of concomitant infection in AIDS and murine AIDS
批准号:
10045068
负责人:
YOSHIKAI Yasunobu
金额:
$2.05万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B).
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999
中文摘要
LP-BM5murine leukemia virus(MuLV)injection is a causative of murine AIDS(MAIDS),characterized by a variety of functional abnormalities of immunocompetent cells and susceptibility to various infectious with Mycobacterium avium or M.bovis BCG as assessed by survival rate and bacterial counts.The expression of IL-15 in the peritoneal macrophages was severely impaired in MAIDS mice following infection with M.bovis BCG。NK cells were increased in the peritoneal cavity of normal mice at earl stage after BCG infection,whereas such increases were not evident in MAIDS mice。Serum IFN-γlevel was also depressed in MAIDS mice following BCG infection.The production IFN-γby T cells from the MAIDS mice infected with M.bovis BCG was significantly lower in response to PPD than that of normal mice infected with M.bovis BCG。These results suggested that depressed IL-15 production in MAIDS mice might be involved in susceptibility against M.bovis BCG.To elucidate the protective roles of IL-15in the progression of MAIDS,we constructed transgenic mice using IL-15cDNA under the control of an MHC class I promoter.The IL-15 Tg mice constitutionally produced a significant level of IL-15 protein and had markedly increased numbers of memory type(CD 44 I D 1 high e D 1 Ly 6C I D 1+I D 1)of CD 8 I D 1+D 1 T cells in the LN.These mice showed resistance to LP-BM5infection accompanied by increases in NK cells and memory CD8 I D1+ii D1T cells and enhanced IFN-γproduction.Thus,these findings suggest that IL-15 production is partly responsible for MAIDS progression and that IL-15may be protective for MAIDS and presumably AIDS progression.
英文摘要
LP-BM5 murine leukemia virus (MuLV) injection is a causative of murine AIDS (MAIDS), characterized by a variety of functional abnormalities of immunocompetent cells and susceptibility to various infectious with Mycobacterium avium or M. bovis BCG as assessed by survival rate and bacterial counts. The expression of IL-15 in the peritoneal macrophages was severely impaired in MAIDS mice following infection with M. bovis BCG. NK cells were increased in the peritoneal cavity of normal mice at earl stage after BCG infection, whereas such increases were not evident in MAIDS mice. Serum IFN-γ level was also depressed in MAIDS mice following BCG infection. The production IFN-γ by T cells from the MAIDS mice infected with M. bovis BCG was significantly lower in response to PPD than that of normal mice infected with M. bovis BCG. These results suggested that depressed IL-15 production in MAIDS mice might be involved in susceptibility against M. bovis BCG.To elucidate the protective roles of IL-15 in the progression of MAIDS, we constructed transgenic mice using IL-15 cDNA under the control of an MHC class I promoter. The IL-15 Tg mice constitutionally produced a significant level of IL-15 protein and had markedly increased numbers of memory type (CD44ィイD1highィエD1 Ly6CィイD1+ィエD1) of CD8ィイD1+ィエD1T cells in the LN. These mice showed resistance to LP-BM5 infection accompanied by increases in NK cells and memory CD8ィイD1+ィエD1 T cells and enhanced IFN-γ production. Thus, these findings suggest that IL-15 production is partly responsible for MAIDS progression and that IL-15 may be protective for MAIDS and presumably AIDS progression.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
Kimura,K.: "Immunogene therapy for murine fibrosarcoma using IL-15 gene with high translation efficiency."Eur.J.Immunol.. 29. 1532-1542 (1999)
Kimura,K.:“使用具有高翻译效率的 IL-15 基因对小鼠纤维肉瘤进行免疫原治疗。”Eur.J.Immunol.. 29. 1532-1542 (1999)
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通讯作者:
Mokuno, Y: "Prostaglandin E_1 protects against liver injury induced by Escherichia coli infection via a dominant Th2-like response of liver T Cells in mice"Hepatology. 30. 1464-1472 (1999)
Mokuno, Y:“前列腺素 E_1 通过小鼠肝脏 T 细胞的显性 Th2 样反应,防止大肠杆菌感染引起的肝损伤”《肝病学》。
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Host defense against bacterial infection in Notch/IL-7Ralpha axis and CD30L dependent manner.
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批准号:25670213
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项目类别:Grant-in-Aid for Challenging Exploratory Research
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资助金额:$2.5万
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财政年份:2013
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负责人:YOSHIKAI Yasunobu
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依托单位:
The roles of innate T cells in bacterial infection
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批准号:21390130
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$12.06万
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财政年份:2009
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负责人:YOSHIKAI Yasunobu
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依托单位:
The roles of primitive T cells bearing Toll-like receptor in microbial infection.
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批准号:14370091
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$9.54万
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财政年份:2002
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负责人:YOSHIKAI Yasunobu
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依托单位:
Molecular mechanisms for generation and maintenance of memory CD8T cells following bacterial infection.
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批准号:13226036
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项目类别:Grant-in-Aid for Scientific Research on Priority Areas
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资助金额:$38.78万
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财政年份:2001
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负责人:YOSHIKAI Yasunobu
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依托单位:
Analysis of the molecular mechanisms for early host defense against bacterial infection
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批准号:09470076
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$6.85万
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财政年份:1997
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负责人:YOSHIKAI Yasunobu
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依托单位:
The roles of gammadelta T cells in host defense aginst bacterial infection
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批准号:02454191
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$4.29万
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财政年份:1990
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负责人:YOSHIKAI Yasunobu
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依托单位:
Analysis of molecular mechanisms of T cell differentiation
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批准号:62480167
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$4.22万
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财政年份:1987
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负责人:YOSHIKAI Yasunobu
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依托单位:
国内基金
海外基金
牛源非结核分枝杆菌(Nontuberculous Mycobacteria,NTMs)与宿主巨噬细胞(Mφ)相互作用的分子机制研究
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批准号:31272566
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项目类别:面上项目
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资助金额:80.0万元
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批准年份:2012
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负责人:钱爱东
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依托单位: