细胞溶解
CD8型
单克隆抗体
免疫系统
CD3型
生物
细胞毒性T细胞
T细胞
体内
免疫学
脾脏
人口
癌症研究
抗体
T淋巴细胞
分子生物学
体外
医学
生物化学
生物技术
环境卫生
作者
Joshua D.I. Ellenhorn,Hans Schreiber,Jeffrey A. Bluestone
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:1990-04-01
卷期号:144 (7): 2840-2846
被引量:48
标识
DOI:10.4049/jimmunol.144.7.2840
摘要
Abstract The present study was undertaken to determine the mechanism of tumor rejection in mice treated with low dose anti-CD3 mAb. It was found that treated mice developed nonrestricted antitumor cytolytic spleen cells of the Thy-1+, asialo GM-1+, CD4-, CD8- phenotype. Although these cells might play a role in immunopotentiating some immune responses, in vivo depletion studies using anti-asialo GM-1 mAb demonstrated that these cells were not involved in the rejection of the progressor tumor, 1591-PRO4L, by anti-CD3 mAb-treated mice. Mice treated with anti-CD3 did develop lasting tumor specific immunity as demonstrated by their ability to reject PRO4L on tumor rechallenge while being unable to reject an unrelated UV-induced tumor. The specificity of this memory implicated T cells in the response to PRO4L in anti-CD3-treated mice. Using in vivo T cell subset depletion of anti-CD3-treated animals, it was shown that both CD4+ and CD8+ T cells are required for anti-CD3-induced tumor rejection. The CD4+ cells provide helper function and are only required in the early rejection period, whereas CD8+ cells are required throughout the immune response. In fact, examination of rejecting tumors from treated animals revealed the presence of tumor-specific CD8+ cytolytic T cells capable of cytolysis immediately after removal from the rejecting PRO4L tumor. Thus, in vivo treatment with anti-CD3 mAb likely results in the pan-stimulation of the entire T cell population, which enhances the generation of specific CD8+ T cells, which then eliminate the tumor.
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