Molecular basis for immunological disease

免疫疾病的分子基础

• 批准号: 10044303
• 负责人: WATANABE Takeshi
• 金额: $ 6.27万
• 依托单位: KYUSHU UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B).
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10044303/
• 关键词: molecular basis of immune disease; collaborative research; autoimmune disease; antigen receptors; cytokine receptors; NK cell; Fas; immune proteasome; 自己免疫病; 免疫異常; B,T細胞分化; 情報伝達; サイトカイン; 細胞死; 免疫寛容

This project was planned to establish collaborative research programs on Immunology between France and Japan. Several major laboratories in Japan working on various subjects of Immunology have been participated and accomplished collaborative works with various immunology groups in France. Japan side was supported by this grant from Monbusho and French side was supported by CNRS. Major subjects of the collaborative research works were (1) molecular approach to the immunological diseases such as autoimmune diabetes, rheumatoid arthritis and SLE, (2) molecular and cellular analysis of the apoptosis of immune cells, molecular analysis of the Fas-mediated apoptosis, (3) regulation of signal transduction from antigen receptors on T and B cells as well as signal transduction from various co-receptors such CD40, CD72, CD100 etc, (4) molecular biology of NK and NKT cells, (5) molecular analysis of human immunodeficiency and immunological abnormalities, (6) regulation of signal transduction from various kinds of cytokine receptors, (7) functional and molecular analysis of immune proteasome, (8) molecular basis for differentiation and activation of B1 cells which plays a crucial role in the production of auto-antibodies, (9) molecular and cellular analysis of heamatopoietic stem cells, (10) genetic analysis of human HLA. We exchanged many kinds of materials including gene targeting mice, transgenic mice, and many various information. During this program, we had two informative meetings in Japan and France. We had fruitful discussion and exchange of information. We successfully finished this collaborative research program.

该项目计划在法国和日本之间建立免疫学合作研究项目。日本研究免疫学各个学科的几个主要实验室已经参与并与法国的各个免疫学团体完成了合作工作。日本方面得到了文部省的资助，法国方面得到了CNRS的支持。合作研究工作的主要主题是（1）自身免疫性糖尿病、类风湿关节炎和系统性红斑狼疮等免疫疾病的分子方法，（2）免疫细胞凋亡的分子和细胞分析，Fas介导的细胞凋亡的分子分析， （3）T细胞和B细胞上抗原受体信号转导的调节以及CD40、CD72、CD100等各种共受体的信号转导，（4）NK和NKT的分子生物学细胞，（5）人体免疫缺陷和免疫异常的分子分析，（6）各种细胞因子受体信号转导的调节，（7）免疫蛋白酶体的功能和分子分析，（8）B1分化和激活的分子基础在自身抗体的产生中起关键作用的细胞，（9）造血干细胞的分子和细胞分析，（10）人类HLA的遗传分析。我们交流了很多种材料，包括基因打靶小鼠、转基因小鼠，还有很多各种各样的信息。在此计划期间，我们在日本和法国举行了两次信息丰富的会议。我们进行了富有成效的讨论和信息交流。我们成功地完成了这个合作研究项目。

项目成果

Cui, J., Watanabe, N. Taniguchi, M. et al: "Inhibition of T helper cell type 2 cell differentation and immunoglobulin E response by ligand-activated Va14 natural killer T cells"J. Exp. Med.. 190. 783-792 (1999)

Cui, J., Watanabe, N. Taniguchi, M. 等人：“配体激活的 Va14 自然杀伤 T 细胞抑制 T 辅助细胞 2 型细胞分化和免疫球蛋白 E 反应”J.

Nakaseko,C.Saito,T,et al: "CTLA-4 engagement delivers inhibitory signal upon T cell activation in the absence of its tyrosine motif in the cytoplasmic tail."J.Exp.Med.. 190. 765-774 (1999)

Nakaseko,C.Saito,T,et al：“在细胞质尾部缺乏酪氨酸基序的情况下，CTLA-4 参与在 T 细胞激活时传递抑制信号。”J.Exp.Med.. 190. 765-774 (1999

Nakaseko, C. Saito, T, et al: "CTLA-4 engagement delivers inhibitory signal upon T cell activation in the absence of its tyrosine motif in the cytoplasmic tail"J. Exp. Med.. 190. 300-303 (1999)

Nakaseko, C. Saito, T 等人：“在细胞质尾部缺乏酪氨酸基序的情况下，CTLA-4 的参与在 T 细胞激活时传递抑制信号”J.

Nakaseko, C., Saito, T., et al: "CTLA-4 engagement delivers inhibitory signal upon T cell activation in the absence of its tyrosine motif in the cytoplasmic tail"J. Exp. Med.. 190. 765-774 (1999)

Nakaseko, C.、Saito, T. 等人：“在细胞质尾部缺乏酪氨酸基序的情况下，CTLA-4 的参与在 T 细胞激活时传递抑制信号”J.

Shirogane, T. T. Hirano, et al: "Synergistic roles for Pim-1 and c-Myc in STAT3-mediated cell progression and anti-apoptosis"Immunity. 11. 709-719 (1999)

Shirogane, T. T. Hirano 等人：“Pim-1 和 c-Myc 在 STAT3 介导的细胞进展和抗凋亡中的协同作用”免疫。