Molecular mechanism of immune regulation and immune tolerance

免疫调节与免疫耐受的分子机制

• 批准号: 05272103
• 负责人: SASAZUKI Takehiko
• 金额: $ 32.64万
• 依托单位: Kyushu University
• 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: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05272103/
• 关键词: immune regulation; immune tolerance; group of generalization; providing information; information exchanges; international symposium; transgenic mouse; gene knockout mouse; 免疫応答

This project was performed by three groups, 1) Molecular mechanisms of immune regulation ; 2) Molecular mechanisms of immune tolerance, and 3) Molecular mechanisms of immune diseases. These three groups cooperated with each other and the following results were obtained. Molecular mechanisms of immune regulation in immune response to natural antigens were elucidated by investigating the recognition of HLA/peptide complexes by TCRs and the resultant cytokine expression induced by interaction with the TCR.A wide range of subjects related to pathological causation were studied by analyzing the relationships between immune dysfunction and disease on a genetic level. Furthermore, several transgenic and gene knockout mouse such as the IL-2 receptor gamma chain mutant mice, CD3 deficient mouse, a TCR-Tg mouse, and the Lyn kinase and HS1 deficient mice were developed over the course of this project. Several domestic symposia, workshops and international symposia were also organized with the cooperation of individual researchers involved in this project.

该项目由三个小组完成，1）免疫调节的分子机制； 2）免疫耐受的分子机制，3）免疫疾病的分子机制。这三个小组相互合作，取得了以下成果。通过研究TCR对HLA/肽复合物的识别以及与TCR相互作用诱导的细胞因子表达，阐明了天然抗原免疫反应中免疫调节的分子机制。通过在基因水平上分析免疫功能障碍与疾病之间的关系，对与病理因果关系相关的广泛主题进行了研究。此外，在该项目过程中还开发了几种转基因和基因敲除小鼠，例如IL-2受体γ链突变小鼠、CD3缺陷小鼠、TCR-Tg小鼠以及Lyn激酶和HS1缺陷小鼠。在参与该项目的个人研究人员的合作下，还组织了多次国内研讨会、讲习班和国际研讨会。

项目成果

Hori, T., et al.: "Japanese cedar pollinosis and HLA-DP5." Tissue Antigens. (in press). (1996)

Hori, T. 等人：“日本雪松花粉病和 HLA-DP5。”

Hanabuchi S.: "Fas and its ligand in a general mechanism of T cell-mediated cytotoxity." Proc.Natl.Acad.Sci.USA. 91. 4930-4934 (1994)

Hanabuchi S.：“T 细胞介导的细胞毒性的一般机制中的 Fas 及其配体。”

Koide Y.: "Molecular analysis of the pathogenesis of autoimmune insulitis in NOD mice." Tohoku J.Exp.Med.173. 157-170 (1994)

Koide Y.：“NOD 小鼠自身免疫性胰岛炎发病机制的分子分析。”

Inoue,T.: "Distinction of mouse CD^<8+> suppressor effector T cell clones from cytotoxic T cell clones by cytokine production and CD45 isoforms." J.Immunol.150. 2121-2128 (1993)

Inoue,T.：“通过细胞因子产生和 CD45 亚型区分小鼠 CD^8 抑制效应 T 细胞克隆与细胞毒性 T 细胞克隆。”

Taniuchi, I., et al.: "Antigen-receptor induced clonal expansion and delection of lymprocytes are imbaired in the mice lacking HS1 protein, a substrate of the antigen receptor coupled tyrosine kinases." EMBO J.14. 3664-3678 (1995)

Taniuchi, I. 等人：“在缺乏 HS1 蛋白（抗原受体偶联酪氨酸激酶的底物）的小鼠中，抗原受体诱导的克隆扩增和淋巴细胞缺失受到影响。”