Jinushi Masahisa, Hodi F Stephen, Dranoff Glenn
Department of Medical Oncology and Cancer Vaccine Center, Dana-Farber Cancer Institute, Boston, MA, USA.
Immunol Rev. 2008 Apr;222:287-98. doi: 10.1111/j.1600-065X.2008.00618.x.
A comparative analysis of vaccination with irradiated, murine tumor cells engineered to express a large number of immunostimulatory molecules established the superior ability of granulocyte-macrophage colony-stimulating factor (GM-CSF) to evoke potent, specific, and long-lasting anti-tumor immunity. Early stage clinical testing of this vaccination strategy in patients with diverse solid and hematologic malignancies revealed the consistent induction of a coordinated humoral and cellular reaction that effectuated substantial tumor destruction. Nonetheless, most subjects eventually succumbed to progressive disease, implying that additional immune defects remained to be addressed. More detailed investigations of the mechanisms underlying protective immunity in murine systems together with the characterization of the anti-tumor reactions of patients who achieved durable clinical benefits in response to immunotherapy uncovered several pathways that restrain the efficacy of GM-CSF-secreting tumor cell vaccines. These include milk fat globule epidermal growth factor protein-8 expansion of forkhead box protein 3+ regulatory T cells, cytotoxic T-lymphocyte antigen-4-mediated negative costimulation, and soluble major histocompatibility complex class I chain-related protein A suppression of NKG2D-dependent innate and adaptive anti-tumor cytotoxicity. Together, these results define key regulatory circuits that attenuate immune-mediated tumor destruction and suggest novel combinatorial therapies that might enhance the clinical activity of GM-CSF-secreting tumor cell vaccines.
对经基因工程改造以表达大量免疫刺激分子的辐照鼠肿瘤细胞进行疫苗接种的比较分析表明,粒细胞-巨噬细胞集落刺激因子(GM-CSF)在激发强效、特异性和持久抗肿瘤免疫方面具有更强的能力。在患有各种实体和血液系统恶性肿瘤的患者中对这种疫苗接种策略进行的早期临床试验显示,一致诱导了协调的体液和细胞反应,从而实现了大量肿瘤破坏。尽管如此,大多数受试者最终还是死于疾病进展,这意味着仍有其他免疫缺陷有待解决。对小鼠系统中保护性免疫的潜在机制进行更详细的研究,以及对免疫治疗后获得持久临床益处的患者的抗肿瘤反应进行表征,发现了几条限制分泌GM-CSF的肿瘤细胞疫苗疗效的途径。这些途径包括乳脂肪球表皮生长因子蛋白8对叉头框蛋白3+调节性T细胞的扩增、细胞毒性T淋巴细胞抗原4介导的负共刺激,以及可溶性主要组织相容性复合体I类链相关蛋白A对NKG2D依赖性先天性和适应性抗肿瘤细胞毒性的抑制。这些结果共同定义了减弱免疫介导的肿瘤破坏的关键调节回路,并提出了可能增强分泌GM-CSF的肿瘤细胞疫苗临床活性的新型联合疗法。