van Elsas A, Hurwitz A A, Allison J P
Howard Hughes Medical Institute, Cancer Research Laboratory, Department of Molecular and Cellular Biology, University of California, Berkeley 94720-3200, USA.
J Exp Med. 1999 Aug 2;190(3):355-66. doi: 10.1084/jem.190.3.355.
We examined the effectiveness of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) blockade, alone or in combination with a granulocyte/macrophage colony-stimulating factor (GM-CSF)-expressing tumor cell vaccine, on rejection of the highly tumorigenic, poorly immunogenic murine melanoma B16-BL6. Recently established tumors could be eradicated in 80% (68/85) of the cases using combination treatment, whereas each treatment by itself showed little or no effect. Tumor rejection was dependent on CD8(+) and NK1.1(+) cells but occurred irrespective of the presence of CD4(+) T cells. Mice surviving a primary challenge rejected a secondary challenge with B16-BL6 or the parental B16-F0 line. The same treatment regimen was found to be therapeutically effective against outgrowth of preestablished B16-F10 lung metastases, inducing long-term survival. Of all mice surviving B16-BL6 or B16-F10 tumors after combination treatment, 56% (38/68) developed depigmentation, starting at the site of vaccination or challenge and in most cases progressing to distant locations. Depigmentation was found to occur in CD4-depleted mice, strongly suggesting that the effect was mediated by CTLs. This study shows that CTLA-4 blockade provides a powerful tool to enhance T cell activation and memory against a poorly immunogenic spontaneous murine tumor and that this may involve recruitment of autoreactive T cells.
我们研究了细胞毒性T淋巴细胞相关抗原4(CTLA-4)阻断剂单独或与表达粒细胞/巨噬细胞集落刺激因子(GM-CSF)的肿瘤细胞疫苗联合使用,对高致瘤性、低免疫原性的小鼠黑色素瘤B16-BL6排斥反应的有效性。使用联合治疗,80%(68/85)的近期形成的肿瘤能够被根除,而单独使用每种治疗方法几乎没有效果或完全无效。肿瘤排斥反应依赖于CD8(+)和NK1.1(+)细胞,但无论CD4(+) T细胞是否存在都会发生。在初次攻击中存活下来的小鼠能够排斥B16-BL6或亲本B16-F0细胞系的再次攻击。发现相同的治疗方案对预先形成的B16-F10肺转移瘤的生长具有治疗效果,可诱导长期存活。在联合治疗后从B16-BL6或B16-F10肿瘤中存活下来的所有小鼠中,56%(38/68)出现色素脱失,从接种疫苗或攻击部位开始,大多数情况下会发展到远处。在CD4细胞耗竭的小鼠中也发现了色素脱失,这强烈表明该效应是由细胞毒性T淋巴细胞(CTLs)介导的。这项研究表明,CTLA-4阻断剂为增强针对低免疫原性自发小鼠肿瘤的T细胞活化和记忆提供了一种强大的工具,并且这可能涉及自身反应性T细胞的募集。