Tuve Sebastian, Chen Bing-Mae, Liu Ying, Cheng Tian-Lu, Touré Papa, Sow Papa Salif, Feng Qinghua, Kiviat Nancy, Strauss Robert, Ni Shaoheng, Li Zong-Yi, Roffler Steve R, Lieber André
Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
Cancer Res. 2007 Jun 15;67(12):5929-39. doi: 10.1158/0008-5472.CAN-06-4296.
Accumulating data indicate that tumor-infiltrating regulatory T cells (Treg) are present in human tumors and locally suppress antitumor immune cells. In this study, we found an increased Treg/CD8 ratio in human breast and cervical cancers. A similar intratumoral lymphocyte pattern was observed in a mouse model for cervical cancer (TC-1 cells). In this model, systemic Treg depletion was inefficient in controlling tumor growth. Furthermore, systemic CTL-associated antigen-4 (CTLA-4) blockade, an approach that can induce tumor immunity in other tumor models, did not result in TC-1 tumor regression but led to spontaneous development of autoimmune hepatitis. We hypothesized that continuous expression of an anti-CTLA-4 antibody localized to the tumor site could overcome Treg-mediated immunosuppression and locally activate tumor-reactive CD8+ cells, without induction of autoimmunity. To test this hypothesis, we created TC-1 cells that secrete a functional anti-CTLA-4 antibody (TC-1/alphaCTLA-4-gamma1 cells). When injected into immunocompetent mice, the growth of TC-1/alphaCTLA-4-gamma1 tumors was delayed compared with control TC-1 cells and accompanied by a reversion of the intratumoral Treg/CD8 ratio due to an increase in tumor-infiltrating IFNgamma-producing CD8+ cells. When local anti-CTLA-4 antibody production was combined with Treg inhibition, permanent TC-1 tumor regression and immunity was induced. Importantly, no signs of autoimmunity were detected in mice that received local CTLA-4 blockade alone or in combination with Treg depletion.
越来越多的数据表明,肿瘤浸润调节性T细胞(Treg)存在于人类肿瘤中,并在局部抑制抗肿瘤免疫细胞。在本研究中,我们发现人类乳腺癌和宫颈癌中Treg/CD8比值升高。在宫颈癌小鼠模型(TC-1细胞)中观察到了类似的肿瘤内淋巴细胞模式。在该模型中,全身性Treg耗竭在控制肿瘤生长方面效率低下。此外,全身性细胞毒性T淋巴细胞相关抗原4(CTLA-4)阻断,一种在其他肿瘤模型中可诱导肿瘤免疫的方法,并未导致TC-1肿瘤消退,反而导致了自身免疫性肝炎的自发发展。我们推测,定位于肿瘤部位的抗CTLA-4抗体的持续表达可以克服Treg介导的免疫抑制,并在局部激活肿瘤反应性CD8+细胞,而不会诱导自身免疫。为了验证这一假设,我们创建了分泌功能性抗CTLA-4抗体的TC-1细胞(TC-1/αCTLA-4-γ1细胞)。当将其注射到具有免疫活性的小鼠体内时,与对照TC-1细胞相比,TC-1/αCTLA-4-γ1肿瘤的生长延迟,并且由于肿瘤浸润的产生干扰素γ的CD8+细胞增加,肿瘤内Treg/CD8比值发生逆转。当局部抗CTLA-4抗体产生与Treg抑制相结合时,可诱导TC-1肿瘤永久性消退和免疫。重要的是,在单独接受局部CTLA-4阻断或与Treg耗竭联合使用的小鼠中未检测到自身免疫迹象。