Dynamism of immune cells in immune-tissue formation
免疫细胞在免疫组织形成中的动态
基本信息
- 批准号:15078203
- 负责人:
- 金额:$ 64.06万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research on Priority Areas
- 财政年份:2003
- 资助国家:日本
- 起止时间:2003 至 2006
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
This project was intended to reveal the regulation of dynamic trafficking of subset of immune cells by chemokines to form immune-tissues in response to pathogen infection. As a result, the following points were found. 1. myeloid dendritic cells (mDCs) capture and process antigens, transport them from the tissue to the draining lymph nodes (LNs) and act as an antigen presenting cells, whereas plasmacytoid DCs (pDCs) directly migrate into inflamed LNs through HEV to help APC function of mDCs 2. nTreg home to the paracortex area of peripheral LNs through HEV in a CCR7 dependent manner and make cluster with subset of DCs 3. a primary response during re-challenge significantly contributes to memory T cell. Upon re-challenge, the skewed Vb usage and T-cell receptor (TCR) repertoire of pre-existing memory T cells is partly corrected by diversity in a newly primed (primary) T cell population. Importantly, this primary population expands more vigorously in a subsequent antigen encounter. These findings indicate that memory T cell populations evolve over multiple challenges, favoring memory T cells generated in more recent encounters, and suggest that these primary populations have essential roles in the perpetuation of antigen-specific T cell populations.
该项目旨在揭示通过趋化因子对免疫细胞子集的动态运输的调节,以形成对病原体感染的免疫组织。结果,发现了以下几点。 1. myeloid dendritic cells (mDCs) capture and process antigens, transport them from the tissue to the draining lymph nodes (LNs) and act as an antigen presenting cells, whereas plasmacytoid DCs (pDCs) directly migrate into inflamed LNs through HEV to help APC function of mDCs 2. nTreg home to the paracortex area of peripheral LNs through HEV以CCR7依赖的方式,并用DCS 3的子集使群集成为簇。重新挑战期间的主要响应显着有助于记忆T细胞。重新挑战后,偏斜的VB使用率和T-Cell受体(TCR)曲目的预先存在记忆T细胞部分通过新启动(原发性)T细胞种群的多样性进行了纠正。重要的是,在随后的抗原遭遇中,这种初级人群会更剧烈地扩展。这些发现表明,记忆T细胞种群在多种挑战中演变,有利于最近相遇中产生的记忆T细胞,并表明这些主要种群在抗原特异性T细胞群体的持久性中具有重要作用。
项目成果
期刊论文数量(85)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Plasmacytoid DCs help lymph node DCs to induce anti-HSV CTLs.
浆细胞样 DC 帮助淋巴结 DC 诱导抗 HSV CTL。
- DOI:10.1084/jem.20041961
- 发表时间:2005-08-01
- 期刊:
- 影响因子:15.3
- 作者:Yoneyama, H;Matsuno, K;Toda, E;Nishiwaki, T;Matsuo, N;Nakano, A;Narumi, S;Lu, B;Gerard, C;Ishikawa, S;Matsushima, K
- 通讯作者:Matsushima, K
Exacerbation of granuloma formation in interleukin-1 receptor antagonist-deficient mice with impaired cell migration associated with Th2 cytokine production.
在白细胞介素 1 受体拮抗剂缺陷小鼠中,与 Th2 细胞因子产生相关的细胞迁移受损,肉芽肿形成加剧。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Iizasa H;et al.
- 通讯作者:et al.
Combined therapy of transcatheter hepatic arterial embolization with intratumoral dendritic cell infusion for hepatocellula carcinoma : clinical safety.
经导管肝动脉栓塞与瘤内树突状细胞输注联合治疗肝细胞癌:临床安全性。
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:Nakamoto Y;et al.
- 通讯作者:et al.
Tomita S, et al.: "T cell-specific disruption of aryl hydrocarbon receptor nuclear translocator gene causes resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced thymic involution."J.Immunol.. 171. 4113-4120 (2003)
Tomita S 等人:“T 细胞特异性破坏芳基碳氢化合物受体核易位基因,导致对 2,3,7,8-四氯二苯并-对-二恶英诱导的胸腺退化产生抗性。”J.Immunol.. 171. 4113
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Mobilization of Dendritic Cell Precursors Into the Circulation by Administration of MIP-1 a in Mice.
通过在小鼠中施用 MIP-1a 将树突状细胞前体动员到循环中。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Zhang Y;et al.
- 通讯作者:et al.
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MATSUSHIMA Kouji其他文献
Osteopontin identifies a novel profibrotic population of fibroblasts
骨桥蛋白鉴定出一种新型的促纤维化成纤维细胞群
- DOI:
- 发表时间:
2013 - 期刊:
- 影响因子:0
- 作者:
ABE Jun;SHICHINO Shigeyuki;HASHIMOTO Shin-ichi;SHIMAOKA Takeshi;TOMURA Michio;INAGAKI Yutaka;MATSUSHIMA Kouji - 通讯作者:
MATSUSHIMA Kouji
Delayed and aberrant immune reconstitution due to destruction of hematological and immunological niches in the acute and chronic phases of GVHD
由于 GVHD 急性期和慢性期血液学和免疫学生态位的破坏导致免疫重建延迟和异常
- DOI:
- 发表时间:
2011 - 期刊:
- 影响因子:0
- 作者:
野竹剛;瀧伸介;MATSUSHIMA Kouji - 通讯作者:
MATSUSHIMA Kouji
Proposal for the breakdown of increased cancer health care cost and its improvement
关于增加的癌症医疗费用的细分及其改进的建议
- DOI:
10.1093/jjco/hyt015 - 发表时间:
2012 - 期刊:
- 影响因子:2.4
- 作者:
野竹剛;瀧伸介;MATSUSHIMA Kouji;鳥谷部真一;Koinuma N - 通讯作者:
Koinuma N
An anti-CD4 depleting antibody induces transient CD80/CD86 up-regulation on dendritic cells in tumor-bearing mice
抗 CD4 耗竭抗体诱导荷瘤小鼠树突状细胞瞬时 CD80/CD86 上调
- DOI:
- 发表时间:
2016 - 期刊:
- 影响因子:0
- 作者:
UEHA Satoshi;OGIWARA Haru;SHAND Francis;KAKIMI Kazuhiro;ITO Satoru;MATSUSHIMA Kouji - 通讯作者:
MATSUSHIMA Kouji
MATSUSHIMA Kouji的其他文献
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{{ truncateString('MATSUSHIMA Kouji', 18)}}的其他基金
Visualization of osteoblast impairments during bone marrow GVHD
骨髓 GVHD 期间成骨细胞损伤的可视化
- 批准号:
24659216 - 财政年份:2012
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Elucidation of the molecular bases of the generation and maintenance of CTL memory by next generation DNA sequencer
下一代DNA测序仪阐明CTL记忆产生和维持的分子基础
- 批准号:
22390095 - 财政年份:2010
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Studies on molecular mechanisms and therapeutic targets of bone marrow GVHD
骨髓GVHD分子机制及治疗靶点研究
- 批准号:
22659095 - 财政年份:2010
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Analysis of generation and control mechanism of CD8+ T cells by chemokines
趋化因子对CD8 T细胞产生及控制机制的分析
- 批准号:
18209016 - 财政年份:2006
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Molecular dynamics of chemokine receptors in memory T cells
记忆T细胞趋化因子受体的分子动力学
- 批准号:
16390143 - 财政年份:2004
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Functional analysis and the molecular mechanism of CCR5 in the CTL induction.
CCR5在CTL诱导中的功能分析及分子机制。
- 批准号:
14370108 - 财政年份:2002
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Pathophysiological and pharmacological studies on chemokines
趋化因子的病理生理学和药理学研究
- 批准号:
08044263 - 财政年份:1996
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for international Scientific Research
Molecular analysis of inflammation and immune response
炎症和免疫反应的分子分析
- 批准号:
08457104 - 财政年份:1996
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Humanization of mouse anti-human IL-8 antibody and development of anti-inflammatory agent against cytokine regulatory factor, NFkB
小鼠抗人IL-8抗体的人源化和针对细胞因子调节因子NFkB的抗炎剂的开发
- 批准号:
07557031 - 财政年份:1995
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Establishment of pathophysiological role of interleukin 8 and development of its inhibitors
白细胞介素8病理生理学作用的确立及其抑制剂的开发
- 批准号:
06454218 - 财政年份:1994
- 资助金额:
$ 64.06万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)
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