MOLECULAR MECHANISM OF THE THIRD TYPE OF CELL DEATH AND ITS APPLICATION FOR SPECIFIC IMMUNOSUPPRESSIVE THERAPY
MOLECULAR MECHANISM OF THE THIRD TYPE OF CELL DEATH AND ITS APPLICATION FOR SPECIFIC IMMUNOSUPPRESSIVE THERAPY
批准号:
09557048
负责人:
ASANO Yoshihiro
金额:
$7.68万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1999
中文摘要
单克隆抗体(mAb),RE 2,直接杀死激活的淋巴细胞,而无需参与补充一条新颖的死亡之路。目前的研究已被用于澄清这种新颖细胞死亡类型的分子的机制和参与分子的机制,并使用这种mAb来稳定的特定免疫抑制方法。使用表达克隆方法,我们用mAb克隆了基因编码对分子反应的基因。MHC class I molec #(KID1k_D1 and KID1b_D1) were turned out to be target molec #of RE2mAb。However,对KI-D1 K-D1, 11-4.1的抗体,并没有诱导细胞死亡在激活的淋巴细胞。因此,我们认为,与K-D1 k-D1或K-D1 b-K-D1相关的未知分子(s)对这种新颖的细胞死亡类型负有责任。合金--特定的耐受性成功地被切割的辐照度与注射的合金化有关。我们认为,对动物进行了综合治疗,对放射性辐射和RE 2-管理可能会提供一种稳定的容忍指数方法。
英文摘要
A monoclonal antibody (mAb), RE2, directly kill activated lymphocytes without participation of complement through a novel pathway of call death. The present study was carried out to clarify the mechanism of and participating molecules of this novel type of cell death and to establish specific immunosuppressive method using this mAb. Using expression cloning method, we cloned the genes coding for the molecules reactive with the mAb. MHC class I molecules (KィイD1kィエD1 and KィイD1bィエD1) were turned out to be target molecules of RE2 mAb. However, antibody specific to KィイD1kィエD1, 11-4.1, did not induce cell death in the activated lymphocytes. Therefore, we think that the unknown molecule(s) associated with KィイD1kィエD1 or KィイD1bィエD1 is responsible for this novel type of cell death.Alloantigen-specific tolerance was successfully induced by fractionated irradiation together with injection of alloantigen. We think the combined treatment of animals with fractionated irradiation and RE2-administration may provide a stable method of tolerance induction.
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M. Shinomiya, S. Nadano, H. Shinomiya and M. Onji: "In situ characterization of dendritic cells occurring in the islets of nonobese diabetic (NOD) mice during the development of insulitis"Pancreas. (in press). (2000)
M. Shinomiya、S. Nadano、H. Shinomiya 和 M. Onji:“对非肥胖糖尿病 (NOD) 小鼠胰岛炎发展过程中胰岛中出现的树突状细胞进行原位表征”。
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Tan, R. S-P., A. U. Kara, C. Feng, and Y. Asano: "Nitoric oxide is not essential in the protection of Plasmodium berghei blood stage murine malaria infection in IRF-1 (interferon regulatory factor-1) deficient mice"9th International Congress of Parasitolo
Tan、R. S-P.、A. U. Kara、C. Feng 和 Y. Asano:“一氧化氮对于保护 IRF-1(干扰素调节因子 1)缺陷小鼠的伯氏疟原虫血期鼠疟疾感染不是必需的”
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Tan,R.S-P.: "Altered immune response of interferon regulatory factor-1 deficient (IRF-1-/-)mice against Plasmodium berghei blood stage malar"Infect.Immunity. 67. 2277-2283 (1999)
Tan,R.S-P.:“干扰素调节因子-1 缺陷 (IRF-1-/-) 小鼠对伯氏疟原虫血期颧骨的免疫反应发生改变”感染。免疫。
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M. Shinomiya, S.M.F. Akbar, H. Shinomiya and M. Onji: "Transfer of dendritic cells ex vivo stimulated with IFN-γ down-modulates autoimmune diabetes in non-obese (NOD) mice"Clin.Exo.Immunol.. 117. 38-43 (1999)
M. Shinomiya、S.M.F. Akbar、H. Shinomiya 和 M. Onji:“体外转移用 IFN-γ 刺激的树突状细胞可下调非肥胖 (NOD) 小鼠的自身免疫糖尿病”Clin.Exo.Immunol.. 117。 38-43 (1999)
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Tan, R.S-P., C.Feng, Y.Asano, and A.U.Kara: "Altered immune response of interferon regulatory factor-1 deficient (IRF-1^<-/->) mice against Plasmodium berghei blood stage malaria infection."Infect.Immunity. 67. 2277-2283 (1999)
Tan、R.S-P.、C.Feng、Y.Asano 和 A.U.Kara:“干扰素调节因子 1 缺陷 (IRF-1^<-/->) 小鼠对伯氏疟原虫血期疟疾感染的免疫反应发生改变。
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Linkage between innate immunity and adaptive immunity during pahogen infection
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Analysis of adaptive expression of a T cell self-recognizing structure in radiation bone marrow chimeras.
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