Roles of complement and complement receptor in self defense
Roles of complement and complement receptor in self defense
批准号:
03670212
负责人:
KINOSHITA Taroh
金额:
$1.22万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1991
资助国家:
日本
项目状态:
已结题
起止时间:
1991 至 1992
中文摘要
补体在微生物表面上以抗体依赖性和非依赖性方式被激活。C3b分子作为簇沉积在微生物表面上。C3b分子随后降解为iC3b,然后降解为C3dg。这些C3片段作为补体受体的配体在参与自我防御系统的各种细胞上表达。本研究旨在阐明补体及其受体在机体自我防御系统中的作用。我们做了以下发现。1.在经典途径中,C5转化酶C3b结合C4b的特异性Ser残基(人中的Ser 1217和小鼠中的Ser 1213)。我们通过给小鼠注射能够下调小鼠B淋巴细胞上的CR1和CR2并抑制C3d与这些受体结合的单克隆抗体(7G6),评估补体受体CR1和CR2在体液免疫应答中的作用。用7G6处理的动物对有限剂量的胸腺依赖性和非胸腺依赖性抗原的反应非常弱。这些结果阐明了补体受体在抗体应答中的重要作用。
英文摘要
Complement is activated on the surface of microorganisms antibody-dependently and -independently. C3b molecules are deposited on the microbial surfaces as clusters. The C3b molecules are subsequently degraded to iC3b and then to C3dg. These C3 fragments act as ligands of complement receptors expressed on various cells that participate in self defense system. This study aimed to elncidate roles of complement and complement receptors in the self defense system. We made following findings.1. Within the classical pathway C5 convertase C3b binds to specific Ser residue of C4b (Ser 1217 in the human and Ser 1213 in the mouse).2. We evaluated roles of complement receptors CR1 and CR2 in the humoral immune response by injecting mice with monoclonal antibody (7G6) that is capable of down-modulating mouse CR1 and CR2 on B-lymphocytes and of inhibiting C3d-binding to these receptors. Animals treated with 7G6 responded very weakly to the limited doses of thymus-dependent and -independent antigens. These results elarified important roles of complement receptors in antibody response.
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Thyphronitis, E: "Modulation of mouse complement receptor 1 and 2 in vivo suppress antibody responses" J. Immunol. 147. 224-230 (1991)
甲状腺炎,E:“体内调节小鼠补体受体 1 和 2 抑制抗体反应”J.Immunol。
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G.Thyphronitis: "Modulation of mouse complement receptors 1 and 2 suppresses antibody responses in Vino." J.Immunol.147. 224-230 (1991)
G. 甲状腺炎:“调节小鼠补体受体 1 和 2 可抑制 Vino 中的抗体反应。”
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Youn Uck Kim: "Covalent finding of C3b to C4b within the classical complement pathway C5 corvertase." J.Biol.Chem.267. (1992)
Youn Uck Kim:“经典补体途径 C5 皮质酶内 C3b 与 C4b 的共价发现。”
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KINOSHITA,T.: "Biology of complement:the overture." Immunol.Today. 12. 291-295 (1991)
KINOSHITA,T.:“补体生物学:序曲。”
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MORINA,H.: "Distinct rceptor and regulatory properties of recombinant mouse complement receptor 1(CR1)and Crry,the two genetic homologs of human CR1." J.Exp.Med.175. 121-129 (1992)
MORINA, H.:“重组小鼠补体受体 1 (CR1) 和 Crry(人类 CR1 的两种基因同源物)的独特受体和调节特性。”
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共 13 条
Molecular mechanisms and functions of structural changes of protein GPI-anchors
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批准号:21247018
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项目类别:Grant-in-Aid for Scientific Research (A)
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资助金额:$28.79万
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财政年份:2009
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负责人:KINOSHITA Taroh
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依托单位:
Stage specific modifications of GPI anchor in Trypanosoma brucei
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批准号:19390119
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$11.98万
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财政年份:2007
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负责人:KINOSHITA Taroh
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依托单位:
Biosynthesis pathway of GPI anchored proteins.
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批准号:13480194
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$9.54万
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财政年份:2001
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负责人:KINOSHITA Taroh
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依托单位:
Mechanism of biosynthesis of protein GPI anchors.
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批准号:11480166
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项目类别:Grant-in-Aid for Scientific Research (B).
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资助金额:$8.13万
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财政年份:1999
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负责人:KINOSHITA Taroh
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依托单位:
Molecular mechanism of GPI anchir biosynthesis
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批准号:09480151
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$8.19万
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财政年份:1997
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负责人:KINOSHITA Taroh
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依托单位:
Characterization of GPI anchor biosynthesis genes.
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批准号:08458181
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$4.35万
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财政年份:1996
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负责人:KINOSHITA Taroh
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依托单位:
Cloning of a GPI-anchor synthsis gene, PIG-A and characterization of its clinical significanece
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批准号:05102006
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项目类别:Grant-in-Aid for Specially Promoted Research
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资助金额:$104.96万
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财政年份:1993
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负责人:KINOSHITA Taroh
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依托单位:
Structural and Functional Analysis of Complement C3/C5 Convertases.
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批准号:01570233
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.34万
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财政年份:1989
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负责人:KINOSHITA Taroh
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依托单位:
国内基金
海外基金
Complement C6蛋白抑制DNA损伤修复增敏甲状腺乳头状癌放射性碘治疗的作用及其机制
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批准号:--
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项目类别:青年科学基金项目
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资助金额:30万元
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批准年份:2022
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负责人:刘宇佳
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依托单位: