Foy Susan P, Mandl Stefanie J, dela Cruz Tracy, Cote Joseph J, Gordon Evan J, Trent Erica, Delcayre Alain, Breitmeyer James, Franzusoff Alex, Rountree Ryan B
Bavarian Nordic, Inc., 595 Penobscot Dr., Redwood City, CA, 94063, USA.
ExoThera LLC, 675 Olive Street, Menlo Park, CA, 94025, USA.
Cancer Immunol Immunother. 2016 May;65(5):537-49. doi: 10.1007/s00262-016-1816-7. Epub 2016 Mar 10.
The dramatic clinical benefit of immune checkpoint blockade for a fraction of cancer patients suggests the potential for further clinical benefit in a broader cancer patient population by combining immune checkpoint inhibitors with active immunotherapies. The anti-tumor efficacy of MVA-BN-HER2 poxvirus-based active immunotherapy alone or in combination with CTLA-4 checkpoint blockade was investigated in a therapeutic CT26-HER-2 lung metastasis mouse model. MVA-BN-HER2 immunotherapy significantly improved the median overall survival compared to untreated controls or CTLA-4 blockade alone (p < 0.001). Robust synergistic efficacy was achieved with the combination therapy (p < 0.01). Improved survival following MVA-BN-HER2 administration was accompanied by increased tumor infiltration by HER-2-specific cytotoxic T lymphocytes (CTL). These tumor-specific CTL had characteristics similar to antiviral CTL, including strong expression of activation markers and co-expression of IFNγ and TNFα. Combination with CTLA-4 blockade significantly increased the magnitude of HER-2-specific T cell responses, with a higher proportion co-expressing TNFα and/or IL-2 with IFNγ. Furthermore, in mice treated with MVA-BN-HER2 (alone or in combination with CTLA-4 blockade), the inducible T cell co-stimulator (ICOS) protein was expressed predominantly on CD4 and CD8 effector T cells but not on regulatory T cells (T(reg)). In contrast, mice left untreated or treated solely with CTLA-4 blockade harbored elevated ICOS(+) Treg, a phenotype associated with highly suppressive activity. In conclusion, poxvirus-based active immunotherapy induced robust tumor infiltration by highly efficient effector T cells. Combination with CTLA-4 immune checkpoint blockade amplified this response resulting in synergistically improved efficacy. These hypothesis-generating data may help elucidate evidence of enhanced clinical benefit from combining CTLA-4 blockade with poxvirus-based active immunotherapy.
免疫检查点阻断对一部分癌症患者具有显著的临床益处,这表明通过将免疫检查点抑制剂与主动免疫疗法相结合,有可能在更广泛的癌症患者群体中获得进一步的临床益处。在治疗性CT26-HER-2肺转移小鼠模型中,研究了基于MVA-BN-HER2痘病毒的主动免疫疗法单独或与CTLA-4检查点阻断联合使用时的抗肿瘤疗效。与未治疗的对照组或单独使用CTLA-4阻断相比,MVA-BN-HER2免疫疗法显著提高了中位总生存期(p<0.001)。联合治疗实现了强大的协同疗效(p<0.01)。给予MVA-BN-HER2后生存期的改善伴随着HER-2特异性细胞毒性T淋巴细胞(CTL)对肿瘤浸润的增加。这些肿瘤特异性CTL具有与抗病毒CTL相似的特征,包括激活标志物的强表达以及IFNγ和TNFα的共表达。与CTLA-4阻断联合使用显著增加了HER-2特异性T细胞反应的强度,更高比例的细胞同时共表达TNFα和/或IL-2与IFNγ。此外,在用MVA-BN-HER2治疗的小鼠(单独或与CTLA-4阻断联合使用)中,诱导性T细胞共刺激分子(ICOS)蛋白主要表达于CD4和CD8效应T细胞上,而不在调节性T细胞(T(reg))上表达。相比之下,未治疗或仅接受CTLA-4阻断治疗的小鼠中ICOS(+)Treg升高,这是一种与高抑制活性相关的表型。总之,基于痘病毒的主动免疫疗法诱导了高效效应T细胞对肿瘤的强大浸润。与CTLA-4免疫检查点阻断联合使用放大了这种反应,从而协同提高了疗效。这些产生假设的数据可能有助于阐明将CTLA-4阻断与基于痘病毒的主动免疫疗法联合使用可增强临床益处的证据。