DYNAMIC ANALYSIS OF MEMORY T GEELs IN RELAPSE AND CHRONIC PROGRESSION IN THE PATHOGENESIS OF MULTIPLE SCLEROSIS

多发性硬化症发病机制中复发和慢性进展记忆T凝胶的动态分析

基本信息

批准号：
15590875
负责人：
FUJIHARA Kazuo
金额：
$ 2.05万
依托单位：
TOHOKU UNIVERSITY
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：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15590875/
关键词：
multiple sclerosis demyelinating disease optic-spinal MS conventional MS memory T cells CCR7 immunological memory antigen presentation

项目摘要

In multiple sclerosis (MS), immunological memories to cause inflammatory demyelination are renewed and retained for long periods, and they are critically important in the lesion development during relapse and chronic progression of the disease. Recent studies demonstrated that the expression of CCR7, a chemokine receptor, is crucial in memory T cell differentiation and the subset identification. Central memory T cells (cmT, CD45RO+CCR7+) have no meaningful effector function, but are resistant to apoptosis and retain immunological memories. On the other hand, effector memory T cells (emT, CD45RO+CCR7-) efficiently migrate to sites of inflammation, secrete inflammatory cytokines, and become apoptotic.In the present study, we analyzed dynamic state of memory T cells in MS.1.A flow cytometric analysis of memory T cell subsets in the cerebrospinal fluid (CSF) and peripheral blood was conducted in MS, viral meningitis and control. The percentages of emT were higher in CSF than in blood in all groups. The cmT subset was significantly increased in MS than in other groups, suggesting its critical role in relapse of MS.2.We immunohistochemically analyzed the expression and distribution of CCR7 and its ligands CCL19 and CCL21 in the cerebral white matter of autopsied brains of MS and controls. CCR7 was stained positive in some dendritic cells, activated macrophages and lymphocytes localized in the periphery of demyelinated lesions and surrounding regions, which suggests on-going antigen presentation. CCL19 was expressed on the venules around the plaques, and that might contribute to the migration of CCR7+ cells to the MS lesions. Messenges of CCR7 and CCL19 were also increased in the regions, supporting the immunohistochemical findings.3.Memory T cell subsets were flow-cytometrically analyzed in the peripheral blood lymphocytes of MS patients stimulated with myelin basic protein twice. As time went by, the emT subset decreased, while the cmT subset increased.

在多发性硬化症（MS）中，长期续签并保留了引起炎症性脱髓鞘的免疫记忆，它们在复发和疾病的长期进展过程中在病变发展中至关重要。最近的研究表明，趋化因子受体CCR7的表达对于记忆T细胞分化和子集鉴定至关重要。中央记忆T细胞（CMT，CD45RO+CCR7+）没有有意义的效应子功能，但对凋亡具有抵抗力并保留免疫记忆。另一方面，效应记忆T细胞（EMT，CD45RO+CCR7-）有效地迁移到炎症部位，分泌炎症细胞因子并凋亡。脑膜炎和控制。 CSF中EMT的百分比高于所有组的血液。 MS的CMT子集的显着增加，与其他组相比，其在Ms.2的复发中的关键作用。我们在MS和对照组的尸体脑化大脑的脑白质中进行了免疫组织化学分析CCR7及其配体CCL19和CCL21的表达和分布。 CCR7在一些树突状细胞中染色阳性，活化的巨噬细胞和淋巴细胞局部局部固定在脱髓鞘病变和周围区域的周围，这表明持续的抗原表现。 CCL19在斑块周围的静脉上表达，这可能有助于CCR7+细胞向MS病变的迁移。在该地区，CCR7和CCL19的事物也增加了，支持免疫组织化学发现。3。在外周血血液淋巴细胞中对肌蛋白碱性蛋白质刺激的MS患者的外围血液淋巴细胞进行流动性分析。随着时间的流逝，EMT子集减少，而CMT子集则增加。

项目成果

期刊论文数量（156）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Chemokine profile in the cerebrospinal fluid and serum of Vogt-Koyanagi-Harada disease

DOI：
10.1016/j.jneuroim.2004.07.014
发表时间：
2005-01-01
期刊：
JOURNAL OF NEUROIMMUNOLOGY
影响因子：
3.3
作者：
Miyazawa, I;Abe, T;Itoyama, Y
通讯作者：
Itoyama, Y

多発性硬化症

多发性硬化症

DOI：
发表时间：
2021
期刊：
Clinical Neuroscience
影响因子：
0
作者：
久冨木原健二;中原仁
通讯作者：
中原仁

Devic病(neuromyelitis optica)

Devic 病（视神经脊髓炎）

DOI：
发表时间：
2004
期刊：
Modern Physician 24
影响因子：
0
作者：
Misu T;Hashimoto Y. et al.;藤原一男;中島一郎;Hashimoto Y. et al.;藤原一男;宮澤イザベル
通讯作者：
宮澤イザベル

多発性硬化症の治療の進め方対症療法とケアの進め方・生活指導の進め方

如何进行多发性硬化症的治疗如何进行对症治疗和护理/如何进行生活方式指导

DOI：
发表时间：
2004
期刊：
Modern Physician 24
影响因子：
0
作者：
Kawanokuchi;J.;Mizuno;T.;Kato;H.;Mitsuma;N.;Suzumura;A.;藤原一男
通讯作者：
藤原一男

Therapeutic guidelines of neuroimmunological diseases.

神经免疫疾病治疗指南。

DOI：
发表时间：
2004
期刊：
影响因子：
0
作者：
Misu T;小野寺淳一;Nakashima I.;Lennon VA.;Nakamura M.;Nakashima I.;Nakashima I.;Narikawa K;Matsumoto Y;藤原一男;三須建郎;Nakashima I;藤原一男;斎田孝彦;Fujihara K.;Misu T.;Saida T.;Nakashima I.;Narikawa K;Narikawa K.;Takahashi T.;斎田孝彦;Saida T.
通讯作者：
Saida T.