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Mechanisms of tissue injury induced with anti-gp70 autoantibodies

抗gp70自身抗体诱导组织损伤的机制

基本信息

批准号：
07670230
负责人：
MIYAZAWA Masaaki
金额：
$ 1.34万
依托单位：
Kinki University (1996)Mie University (1995)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07670230/
关键词：
Autoantibodies go70 Tissue injury Platelets Endogenous viruses Monoclonal antibody Antigenic epitope 糸球体

项目摘要

1. Mechanisms of the development of glomerular lesions induced by transplantation of anti-gp70 antibody-producing hybridomas : Purified IgG molecules of the nephritogenic anti-gp70 monoclonal antibodies were injected into NZW and C57BL/6 strains of mice. Glomerular lesions were observed only in NZW mice that express a high level of serum gp70. Thus, gp70-anti-gp70 immune complexes seems to be involved in the development of glomerular lesions.2. Localization of antigenic epitopes recognized by nephritogenic anti-gp70 monoclonal antibodies : By expressing chimeras of xenotropic and polytropic viral env genes, antigenic epitopes recognized by most of the nephritogenic anti-gp70 monoclonal antibodies were mapped to the N-terminal one third of the xenotropic viral gp70.3. Expression of endogenous retroviral env gene products on platelets : Some of the pathogenic anti-gp70 monoclonal antibodies induce thrombocytopenia associated with systemic hemorrhage when injected into normal mice. Therefore, possible expression of endogenous retroviral gp70 on platelets was tested by FACS analysis. Peripheral blood platelets of normal and MRL strains of mice express several different endogenous retroviral env gene products on their surface. Platelets were aggregated in vivo in small vessels as demonstrated by electron microscopic examination of antibody-injected mice.

1.产生抗gp 70抗体的杂交瘤的移植诱导的肾小球病变的发展机制：将致肾炎性抗gp 70单克隆抗体的纯化IgG分子注射到NZW和C57 BL/6品系小鼠中。仅在表达高水平血清gp 70的NZW小鼠中观察到肾小球病变。因此，gp 70-抗gp 70免疫复合物似乎参与了肾小球病变的发展。致肾性抗gp 70单克隆抗体识别的抗原表位的定位：通过表达异嗜性和多嗜性病毒env基因的嵌合体，大多数致肾性抗gp 70单克隆抗体识别的抗原表位被定位到异嗜性病毒gp70.3的N-末端三分之一。内源性逆转录病毒env基因产物在血小板上的表达：当注射到正常小鼠中时，一些致病性抗gp 70单克隆抗体诱导与全身出血相关的血小板减少症。因此，通过FACS分析测试血小板上内源性逆转录病毒gp 70的可能表达。正常和MRL小鼠品系的外周血血小板在其表面表达几种不同的内源性逆转录病毒env基因产物。如通过抗体注射小鼠的电子显微镜检查所证明的，血小板在体内聚集在小血管中。