Mechanism of tumor rejection in anti-CD3 monoclonal antibody-treated mice.

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]
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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