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重新审视A2G小鼠中的病毒溶瘤作用:单克隆抗体介导的肿瘤排斥反应。

Viral oncolysis in the A2G mouse revisited: monoclonal antibody-mediated tumor rejection.

作者信息

Klein P A

机构信息

Department of Pathology, College of Medicine, University of Florida, Gainesville 32610.

出版信息

J Interferon Res. 1987 Oct;7(5):583-9. doi: 10.1089/jir.1987.7.583.

DOI:10.1089/jir.1987.7.583
PMID:3681014
Abstract

A2G mice can be immunized against the Ehrlich ascites tumor (EAT) by influenza virus oncolysis or with influenza virus oncolysates. To facilitate studies of the cellular antigens immunopotentiated by viral oncolysis, monoclonal antibodies (mAbs) against EAT cells were produced from postoncolytic EAT-immune A2G mice. Reciprocal competitive binding on EAT cells was used to classify the mAbs into epitope-related groups. One mAb, 198.9, could fully protect A2G mice against EAT cell challenge, could rescue A2G mice from an established EAT, and could mediate lysis of EAT cells in vivo. mAb 198.9 provides a new tool for studying the biochemical characteristics and immunological properties of a cellular antigen centrally involved in this model.

摘要

A2G小鼠可以通过流感病毒溶瘤或使用流感病毒溶瘤产物来免疫抵抗艾氏腹水瘤(EAT)。为便于研究病毒溶瘤增强免疫的细胞抗原,从经溶瘤后的EAT免疫A2G小鼠中制备了抗EAT细胞的单克隆抗体(mAb)。利用在EAT细胞上的相互竞争结合将这些mAb分类为表位相关组。一种mAb,即198.9,能完全保护A2G小鼠免受EAT细胞攻击,能使已患EAT的A2G小鼠康复,并能在体内介导EAT细胞的裂解。mAb 198.9为研究该模型中核心细胞抗原的生化特性和免疫特性提供了一种新工具。

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