Complement receptors (CR) and cytotoxic responses: monoclonal antibodies directed against CR1 and CR3 inhibit the generation of human allospecific and virus specific cytotoxic cells in vitro.

G Inghirami, J D Lambris, G C Tsokos
{"title":"Complement receptors (CR) and cytotoxic responses: monoclonal antibodies directed against CR1 and CR3 inhibit the generation of human allospecific and virus specific cytotoxic cells in vitro.","authors":"G Inghirami,&nbsp;J D Lambris,&nbsp;G C Tsokos","doi":"10.3109/08923978609031086","DOIUrl":null,"url":null,"abstract":"<p><p>A variety of cellular immune responses involve complement factors which bind to specific receptors, and modulate or effect a specific reaction. Monoclonal antibodies (MAb) have been generated against complement receptors (CR) 1 and 3, which were utilized to investigate human allogeneic and Epstein-Barr virus specific cytotoxic cells in vitro. MAb OKM1, which binds to the C3bi CR (CR3), and MAb M710, which binds to the C3b/4b CR (CR1), inhibited the generation of both allogeneic and virus specific cytotoxic responses in vitro in a dose-dependent way; doses of 1 microgram/ml (or greater) completely abrogated the cytotoxic responses. Inhibition of these responses was observed when the MAb was added to the cultures at any time point except the last two days. In addition, treatment of the responder (but not the stimulator cells) with either MAb resulted in complete inhibition of cytotoxic responses. These experiment indicate that complement receptors participate in the generation of human cytotoxic responses in vitro.</p>","PeriodicalId":16049,"journal":{"name":"Journal of immunopharmacology","volume":"8 1","pages":"75-88"},"PeriodicalIF":0.0000,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/08923978609031086","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of immunopharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/08923978609031086","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

A variety of cellular immune responses involve complement factors which bind to specific receptors, and modulate or effect a specific reaction. Monoclonal antibodies (MAb) have been generated against complement receptors (CR) 1 and 3, which were utilized to investigate human allogeneic and Epstein-Barr virus specific cytotoxic cells in vitro. MAb OKM1, which binds to the C3bi CR (CR3), and MAb M710, which binds to the C3b/4b CR (CR1), inhibited the generation of both allogeneic and virus specific cytotoxic responses in vitro in a dose-dependent way; doses of 1 microgram/ml (or greater) completely abrogated the cytotoxic responses. Inhibition of these responses was observed when the MAb was added to the cultures at any time point except the last two days. In addition, treatment of the responder (but not the stimulator cells) with either MAb resulted in complete inhibition of cytotoxic responses. These experiment indicate that complement receptors participate in the generation of human cytotoxic responses in vitro.

补体受体(CR)和细胞毒性反应:针对CR1和CR3的单克隆抗体在体外抑制人类异体特异性和病毒特异性细胞毒性细胞的产生。
多种细胞免疫反应涉及到与特定受体结合的补体因子,并调节或影响特定反应。制备了针对补体受体(CR) 1和3的单克隆抗体(MAb),用于体外检测人同种异体和eb病毒特异性细胞毒细胞。与C3bi CR (CR3)结合的单抗OKM1和与C3b/4b CR (CR1)结合的单抗M710在体外以剂量依赖的方式抑制异体和病毒特异性细胞毒性反应的产生;1微克/毫升(或更大)的剂量完全消除细胞毒性反应。除最后两天外,在任何时间点将MAb添加到培养物中都可以观察到这些反应的抑制作用。此外,用任一单抗治疗应答细胞(而非刺激细胞)均可完全抑制细胞毒性反应。这些实验表明,补体受体参与体外人细胞毒性反应的产生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信