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利用工程化溶瘤痘苗病毒重塑肿瘤微环境可改善 PD-L1 抑制效果。

Remodeling of the tumor microenvironment using an engineered oncolytic vaccinia virus improves PD-L1 inhibition outcomes.

机构信息

Department of Laboratory Medicine, Hangzhou Ninth People's Hospital, Hangzhou, China.

Department of Hematology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.

出版信息

Biosci Rep. 2021 Jun 25;41(6). doi: 10.1042/BSR20204186.

DOI:10.1042/BSR20204186
PMID:34060602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8193643/
Abstract

Immune checkpoint inhibitor (ICI) immunotherapies have vastly improved therapeutic outcomes for patients with certain cancer types, but these responses only manifest in a small percentage of all cancer patients. The goal of the present study was to improve checkpoint therapy efficacy by utilizing an engineered vaccinia virus to improve the trafficking of lymphocytes to the tumor, given that such lymphocyte trafficking is positively correlated with patient checkpoint inhibitor response rates. We developed an oncolytic vaccinia virus (OVV) platform expressing manganese superoxide dismutase (MnSOD) for use as both a monotherapy and together with anti-PD-L1. Intratumoral OVV-MnSOD injection in immunocompetent mice resulted in inflammation within poorly immunogenic tumors, thereby facilitating marked tumor regression. OVV-MnSOD administration together with anti-PD-L1 further improved antitumor therapy outcomes in models in which these monotherapy approaches were ineffective. Overall, our results emphasize the value of further studying these therapeutic approaches in patients with minimally or non-inflammatory tumors.

摘要

免疫检查点抑制剂 (ICI) 免疫疗法极大地改善了某些癌症类型患者的治疗效果，但这些反应仅在所有癌症患者中的一小部分中表现出来。本研究的目的是通过利用工程化的牛痘病毒来改善淋巴细胞向肿瘤的转运，从而提高检查点治疗的疗效，因为这种淋巴细胞转运与患者的检查点抑制剂反应率呈正相关。我们开发了一种表达锰超氧化物歧化酶 (MnSOD) 的溶瘤牛痘病毒 (OVV) 平台，用作单一疗法以及与抗 PD-L1 联合使用。在免疫功能正常的小鼠中瘤内注射 OVV-MnSOD 会导致免疫原性差的肿瘤内炎症，从而促进明显的肿瘤消退。OVV-MnSOD 联合抗 PD-L1 治疗进一步改善了这些单药治疗方法无效的模型中的抗肿瘤治疗效果。总体而言，我们的研究结果强调了在最小或非炎症性肿瘤患者中进一步研究这些治疗方法的价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/977f512eccf7/bsr-41-bsr20204186-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/bc829a23f866/bsr-41-bsr20204186-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/6b38416eaf44/bsr-41-bsr20204186-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/7efb481bf7d3/bsr-41-bsr20204186-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/977f512eccf7/bsr-41-bsr20204186-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/bc829a23f866/bsr-41-bsr20204186-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/6b38416eaf44/bsr-41-bsr20204186-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/7efb481bf7d3/bsr-41-bsr20204186-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f10/8193643/977f512eccf7/bsr-41-bsr20204186-g4.jpg

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Oncoimmunology. 2020 May 22;9(1):1761229. doi: 10.1080/2162402X.2020.1761229.
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Embelin Promotes Oncolytic Vaccinia Virus-Mediated Antitumor Immunity Through Disruption of IL-6/STAT3 Signaling in Lymphoma.紫铆因通过破坏淋巴瘤中的IL-6/STAT3信号传导促进溶瘤痘苗病毒介导的抗肿瘤免疫。
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Cancer-Associated Fibroblasts Promote Immunosuppression by Inducing ROS-Generating Monocytic MDSCs in Lung Squamous Cell Carcinoma.
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