Linkage between innate immunity and adaptive immunity during pahogen infection

病原体感染期间先天免疫和适应性免疫之间的联系

基本信息

  • 批准号:
    14207012
  • 负责人:
  • 金额:
    $ 24.88万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 财政年份:
    2002
  • 资助国家:
    日本
  • 起止时间:
    2002 至 2005
  • 项目状态:
    已结题

项目摘要

Pathogenic infections lead to activation of innate immunity followed by induction of a Th1 T cell subset. However, the mechanism in this shift has not been clarified. We used DO 11.10 OVA-specific TCR-TG mouse T cell and the intracellular infectious pathogen Listeria monocytogenes (Lm) to evaluate the effect of pathogenic infections. We investigated genes that involved in the host-pathogen interaction and is required for the initiation of T cell subset differentiation in the early phase of pathogen infection. We show in this report that toll like receptor (TLR)-2, TLR-4 and MyD88 molecules are not essentially required for the induction of Th1 differentiation during Lm infection. It is also shown that genes involved in the expression of the pathogenicity of Lm are not required for the induction of Th1. We checked the mutant strain of Lm which were disrupted gene by insertion of transposon or temperature sensitive plasmid. We evaluated the mutant for determining gene(s) responsible for inducing T cell shift. We found the mutants of Lm lost either the ability of Th1 induction or the inhibition of Th2 induction, suggesting that the induction of Th1 subset and the inhibition of Th2 subset induction are separate phenomenon and are influenced by distinct genes carried by Lm genome.
病原性感染导致先天免疫的激活,随后诱导Th 1 T细胞亚群。然而,这种转变的机制尚未阐明。我们使用DO 11.10 OVA特异性TCR-TG小鼠T细胞和细胞内感染性病原体单核细胞增生李斯特菌(Lm)来评估病原性感染的效果。我们研究了参与宿主-病原体相互作用的基因,以及在病原体感染的早期阶段启动T细胞亚群分化所需的基因。我们在这份报告中表明,Toll样受体(TLR)-2,TLR-4和MyD 88分子并不是Lm感染过程中诱导Th 1分化所必需的。它还表明,参与Lm的致病性的表达的基因是不需要的诱导Th 1。我们检查了通过插入转座子或温度敏感性质粒来破坏基因的Lm突变株。我们评估了突变体用于确定负责诱导T细胞移位的基因。我们发现Lm突变体的Th 1诱导能力和Th 2诱导抑制能力均丧失,提示Lm基因组中Th 1亚群的诱导和Th 2亚群的诱导抑制是两种不同的现象,受不同基因的影响。

项目成果

期刊论文数量(58)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Shinomiya, H., et al.: "Preparation and characterization of recombinant murine p65/L-plastin expressed in E. coli and high-titer antibodies against the protein"Biosci. Biotechnol. Biochem.. (in press). (2003)
Shinomiya, H. 等人:“在大肠杆菌中表达的重组鼠 p65/L-plastin 的制备和表征以及针对该蛋白质的高滴度抗体”Biosci。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Analysis of a bacterial lipopolysaccharide-activated serine kinase that posphorylates p65/L-plastin in macrophages
分析巨噬细胞中 p65/L-plastin 磷酸化的细菌脂多糖激活丝氨酸激酶
Evaluation of mitogen-induced responses in marine mammal and human lymphocytes by in-vitro exposure of butyltins and non-ortho coplanar PCBs.
  • DOI:
    10.1016/s0269-7491(02)00155-0
  • 发表时间:
    2002-12
  • 期刊:
  • 影响因子:
    8.9
  • 作者:
    H. Nakata;Akihito Sakakibara;M. Kanoh;S. Kudo;H. Watanabe;N. Nagai;N. Miyazaki;Y. Asano;S. Tanabe
  • 通讯作者:
    H. Nakata;Akihito Sakakibara;M. Kanoh;S. Kudo;H. Watanabe;N. Nagai;N. Miyazaki;Y. Asano;S. Tanabe
X-ray solution scattering study on the leukocyte-specific EF-hand proteins,p65/L-plastin and grancalcin.
白细胞特异性 EF-hand 蛋白、p65/L-plastin 和 grancalcin 的 X 射线溶液散射研究。
Identification of interferon regulatory factor (IRF)-1 binding site in IL-12 p40 gene promoter.
IL-12 p40 基因启动子中干扰素调节因子 (IRF)-1 结合位点的鉴定。
  • DOI:
  • 发表时间:
    2003
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Maruyama;S.;et al.
  • 通讯作者:
    et al.
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ASANO Yoshihiro其他文献

ASANO Yoshihiro的其他文献

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{{ truncateString('ASANO Yoshihiro', 18)}}的其他基金

Elucidation of the irreversible mechanism of severe heart failure using biological monitoring murine heart failure model
利用生物监测小鼠心力衰竭模型阐明严重心力衰竭的不可逆机制
  • 批准号:
    15K09139
  • 财政年份:
    2015
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
A novel function of Interferon regulatory factor-1
干扰素调节因子-1的新功能
  • 批准号:
    24659475
  • 财政年份:
    2012
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Development of nursing process engine based on nursing data mapping
基于护理数据映射的护理流程引擎开发
  • 批准号:
    21592679
  • 财政年份:
    2009
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
A Study for Epigenetic Regulation to Maintain Cardiac Homeostasis
表观遗传调控维持心脏稳态的研究
  • 批准号:
    21689022
  • 财政年份:
    2009
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Young Scientists (A)
The 2nd pathway of T cell subset differentiation induced by pathogenic infection
病原体感染诱导T细胞亚群分化的第二条途径
  • 批准号:
    10470086
  • 财政年份:
    1998
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
APPROACHES FOR CONTROLLING INFECTION BY GENE THERAPY
通过基因治疗控制感染的方法
  • 批准号:
    10044299
  • 财政年份:
    1998
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
MOLECULAR MECHANISM OF THE THIRD TYPE OF CELL DEATH AND ITS APPLICATION FOR SPECIFIC IMMUNOSUPPRESSIVE THERAPY
第三类细胞死亡的分子机制及其在特异性免疫抑制治疗中的应用
  • 批准号:
    09557048
  • 财政年份:
    1997
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
DEVELOPMENT OF MATERIALS WHICH HAVE INHIBITORY ACTIVITY ON GRAFT-VERSUS-HOST DISEASE ACCOPANIED BY BONE MARROW TRANSPLANTATION
对骨髓移植伴随的移植物抗宿主病具有抑制活性的材料的开发
  • 批准号:
    05557032
  • 财政年份:
    1993
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for Developmental Scientific Research (B)
Analysis of mediators which regulate T-T cell interactions involved in regulatory immune responses.
分析调节参与调节性免疫反应的 T-T 细胞相互作用的介质。
  • 批准号:
    01480187
  • 财政年份:
    1989
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Analysis of adaptive expression of a T cell self-recognizing structure in radiation bone marrow chimeras.
放射骨髓嵌合体中 T 细胞自我识别结构的适应性表达分析。
  • 批准号:
    61480155
  • 财政年份:
    1986
  • 资助金额:
    $ 24.88万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)

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先天免疫中线性泛素信号传导的调节
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    2024
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Elucidating the Intricate Interplay between Mitochondria, Innate Immunity, and Viral Pathogenesis in Heart Failure
阐明心力衰竭中线粒体、先天免疫和病毒发病机制之间复杂的相互作用
  • 批准号:
    491149
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    2023
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Syudy 论高致病性禽流感感染的先天免疫
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Radioresistant Innate Immunity in SAVI Tissue-Specific Autoinflammation
SAVI 组织特异性自身炎症中的抗辐射先天免疫
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开发一种新的治疗策略,通过激活先天免疫来克服小细胞肺癌的多药耐药性
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    2023
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生命早期肺部感染、微生物组和经过训练的先天免疫
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ADAM9 在病毒 RNA 传感和抗病毒先天免疫中的作用
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