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Analysis of the mechanism for the regulation of antibody responses by inflammation-associated remodeling of lymph nodes

Analysis of the mechanism for the regulation of antibody responses by inflammation-associated remodeling of lymph nodes
炎症相关淋巴结重塑调节抗体反应的机制分析
批准号:
23790525
负责人:
ABE Jun
金额:
$2.75万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2012

项目摘要

项目成果

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中文摘要
翻译
在这项研究中,我试图阐明淋巴(LN)重塑调节抗体反应的机制。通过这项研究,我获得了以下认识:1)LN间质网络的分子组成与LN T细胞区的分子组成非常相似;2)抗原非特异性B细胞介导的LN髓质重塑调节抗原特异性抗体反应;3)纤维母细胞网状细胞(FRC)激活后,作为LN间质网络的主要细胞类型,在不增加数量的情况下经历周转;4)激活的FRC促进抗原特异性辅助T细胞反应的收缩,从而影响滤泡辅助T细胞的数量。
英文摘要
In this study, I sought to clarify the mechanism for the regulation of antibody responses by lymph node (LN) remodeling. I obtained the following insights through this study: 1) Molecular components of stromal network in LN medulla resembled closely to those in T cell region of the LN; 2) Medullary remodeling of LN mediated by antigen-non-specific B cells regulate the antigen-specific antibody response; 3) Upon activation, fibroblastic reticular cells (FRCs), the major cell type shaping the LN stromal network, undergo the turnover without expansion of their number; 4) Activated FRCs promote the contraction of antigen-specific helper T cell response, thereby affecting the number of follicular helper T cells.
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Cognate and non-cognate B cells mediate the remodeling of lymph node medulla that contributes to antibody responses
同源和非同源 B 细胞介导淋巴结髓质重塑,从而促进抗体反应
DOI: --
发表时间: 2011
期刊:
影响因子: --
作者: [Jun Abe, Satoshi Ueha, Yusuke Shono, Makoto Kurachi, Michio Tomura, Kazuhiro Kakimi, and Kouji Matsushima]
通讯作者: and Kouji Matsushima
DOI: 10.4049/jimmunol.1202267
发表时间: 2013-04-15
期刊: JOURNAL OF IMMUNOLOGY
影响因子: 4.4
作者: [Hashimoto, Shin-ichi, Ogoshi, Katsumi, Matsushima, Kouji]
通讯作者: Matsushima, Kouji
DOI: 10.1093/intimm/dxr089
发表时间: 2012-01-01
期刊: INTERNATIONAL IMMUNOLOGY
影响因子: 4.4
作者: [Abe, Jun, Ueha, Satoshi, Matsushima, Kouji]
通讯作者: Matsushima, Kouji
Chemokine receptor CXCR3 facilitates CD8(+) T cell differentiation into short-lived effector cells leading to memory degeneration.
趋化因子受体CXCR3促进CD8(+)T细胞分化为短寿命的效应细胞,导致记忆变性。
DOI: 10.1084/jem.20102101
发表时间: 2011-08-01
期刊: The Journal of experimental medicine
影响因子: --
作者: [Kurachi M, Kurachi J, Suenaga F, Tsukui T, Abe J, Ueha S, Tomura M, Sugihara K, Takamura S, Kakimi K, Matsushima K]
通讯作者: Matsushima K
7
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    • 批准号:
      23580019
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
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    • 财政年份:
      2011
    • 负责人:
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    • 项目类别:
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    • 资助金额:
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    • 财政年份:
      2011
    • 负责人:
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    • 依托单位:
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