Role of SLC and ELC chemokines in the development of experimental allergic encephalomyelitis as an animal model of multiple sclerosis.
SLC 和 ELC 趋化因子在多发性硬化症动物模型实验性过敏性脑脊髓炎发展中的作用。
基本信息
- 批准号:15590911
- 负责人:
- 金额:$ 2.24万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2003
- 资助国家:日本
- 起止时间:2003 至 2004
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Experimental allergic encephalomyelitis(EAE) is an animal model for multiple sclerosis. C57BL/6 mouse immunized subcutaneously with myelin oligodendrocyte glycoprotein(MOG) 35-55 peptide(MOG35-55 peptide) in CFA developed EAE. However, C57BL/6-plt/plt mouse did not develop EAE, when similarly treated. plt mouse has a defect in the expression of CCL19/CCL21. Thus, it is possible that these chemokines are involved in the development of EAE. There were two possibilities ; one was the migration failure of pathogenic T cells into CNS, the other was that pathogenic T cells were not generated in the plt mouse. To differentiate these possibilities, T cells from C57BL/6 wild type mice immunized with MOG35-55 peptide in CFA were intravenously transferred into plt mice, which resulted in the development of EAE in plt mice. When draining lymph node cells from these mice intravenously immunized with MOG peptide in CFA, were stimulated in vitro with the peptide, T cells from plt mice produced much more IL-4 than those from wild type mice, whereas IFN-γ was inversely produced. These results, although the experiments were still preliminary, suggested that CCL19/CCL21 are involved in the generation of pathogenic Th1 cells for EAE induction. The mechanisms for the involvement of these chemokines are now under the investigation.
实验性变态反应性脑脊髓炎(EAE)是多发性硬化症的动物模型。用CFA中的髓鞘少突胶质细胞糖蛋白(MOG)35-55肽(MOG 35 - 55肽)皮下免疫C57 BL/6小鼠产生EAE。然而,C57 BL/6-plt/plt小鼠在类似处理时未发生EAE。plt小鼠存在CCL 19/CCL 21表达缺陷。因此,这些趋化因子可能参与EAE的发展。有两种可能:一是致病性T细胞向中枢神经系统迁移失败,二是plt小鼠体内未产生致病性T细胞。为了区分这些可能性,将来自用CFA中的MOG 35 -55肽免疫的C57 BL/6野生型小鼠的T细胞静脉内转移到plt小鼠中,这导致plt小鼠中EAE的发展。当用CFA中的MOG肽静脉内免疫的这些小鼠的引流淋巴结细胞在体外用肽刺激时,来自plt小鼠的T细胞产生比来自野生型小鼠的T细胞多得多的IL-4,而IFN-γ产生相反。这些结果,虽然实验仍然是初步的,表明CCL 19/CCL 21参与了EAE诱导的致病性Th 1细胞的产生。这些趋化因子参与的机制目前正在调查中。
项目成果
期刊论文数量(32)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yoshino M, Yamazaki H, Nakano H, Kakiuchi T, Ryoke K, Kunisada T, Hayashi S: "Distinct antigen trafficking from skin in the steady and active states"Int Immunol. 15(6). 773-779 (2003)
Yoshino M、Yamazaki H、Nakano H、Kakiuchi T、Ryoke K、Kunisada T、Hayashi S:“稳定和活跃状态下皮肤中的不同抗原贩运”Int Immunol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Selective enhancement of B cell antigen receptor-mediated antigen presentation by treatment with transforming growth factor-beta.
通过转化生长因子-β 治疗选择性增强 B 细胞抗原受体介导的抗原呈递。
- DOI:
- 发表时间:2003
- 期刊:
- 影响因子:0
- 作者:Arai C;Ichijo T;Tanaka Y;Okada Y;Umeda M;Uchida T;Kiniwa M;Kakiuchi T.
- 通讯作者:Kakiuchi T.
CCR7 signals are essential for cortex-medulla migration of developing thymocytes.
CCR7信号对于发育中的胸腺细胞的皮层迁移至关重要。
- DOI:10.1084/jem.20040643
- 发表时间:2004-08-16
- 期刊:
- 影响因子:15.3
- 作者:Ueno, T;Saito, F;Gray, DHD;Kuse, S;Hieshima, K;Nakano, H;Kakiuchi, T;Lipp, M;Boyd, RL;Takahama, Y
- 通讯作者:Takahama, Y
Localization of marginal zone macrophages is regulated by C-C chemokine ligands 21/19
- DOI:10.4049/jimmunol.173.8.4815
- 发表时间:2004-10-15
- 期刊:
- 影响因子:4.4
- 作者:Ato, M;Nakano, H;Kaye, PM
- 通讯作者:Kaye, PM
Role of CCL21 in Recruitment of T Precursor Cells to Fetal Thymus.
CCL21 在 T 前体细胞募集至胎儿胸腺中的作用。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Liu C;Ueno T;Kuse S;Saito F;Nitta T;Piali L;Nakano H;Kakiuchi T;Lipp M;Hollander GA;Takahama Y.
- 通讯作者:Takahama Y.
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KAKIUCHI Terutaka其他文献
KAKIUCHI Terutaka的其他文献
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{{ truncateString('KAKIUCHI Terutaka', 18)}}的其他基金
Role of chemokine CCL19/21 in the development of experimental autoimmune encephalomyelitis
趋化因子 CCL19/21 在实验性自身免疫性脑脊髓炎发生中的作用
- 批准号:
19591013 - 财政年份:2007
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Role of CCL19/ 21 chemokine in the development of experimental autoimmune encephalomyelitis
CCL19/21趋化因子在实验性自身免疫性脑脊髓炎发生中的作用
- 批准号:
17590900 - 财政年份:2005
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Failure to induce experimental allergic encephalitis in mice lucking expression of SLC chemokine.
未能在幸运表达 SLC 趋化因子的小鼠中诱发实验性过敏性脑炎。
- 批准号:
12670621 - 财政年份:2000
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
MECHANISMS FOR THE INHIBITION OF DEVELOPMENT IN ENCEPHALOMYELITIS IN MICE LACKING THE EXPRESSION OF A CHEMOKINE REQUIRED FOR T CELL MIGRATION.
抑制缺乏 T 细胞迁移所需趋化因子表达的小鼠脑脊髓炎发展的机制。
- 批准号:
10670606 - 财政年份:1998
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)