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CXCL2与HVJ-E联合使用可抑制乳腺癌的肿瘤生长和肺转移，并增强抗PD-1抗体疗法。

CXCL2 combined with HVJ-E suppresses tumor growth and lung metastasis in breast cancer and enhances anti-PD-1 antibody therapy.

作者信息

Pan Yi Chun, Nishikawa Tomoyuki, Chang Chin Yang, Tai Jiayu A, Kaneda Yasufumi

机构信息

Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.

Department of Device Application for Molecular Therapeutics, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.

出版信息

Mol Ther Oncolytics. 2020 Dec 25;20:175-186. doi: 10.1016/j.omto.2020.12.011. eCollection 2021 Mar 26.

DOI:10.1016/j.omto.2020.12.011
PMID:33575480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7851488/
Abstract

Breast cancer has a high risk of metastasis; however, no effective treatment has been established. We developed a novel immunotherapy for breast cancer to enhance cytotoxic T lymphocytes against cancer cells using N1-type neutrophils with anti-tumor properties. For this purpose, we combined CXCL2 (CXC chemokine ligand 2) plasmid DNA with inactivated Sendai virus (hemagglutinating virus of Japan)-envelope (HVJ-E). The combination of CXCL2 DNA and HVJ-E (C/H) suppressed the growth of murine breast cancers in orthotopic syngeneic models by enhancing cytotoxic T lymphocytes and inhibited lung metastasis of breast cancer from primary lesions. N1-type neutrophils (CD11b Ly6G FAS) increased in the tumor microenvironment with C/H treatment, and tumor suppression and cytotoxic T lymphocyte activation from C/H was blocked after administrating anti-neutrophil antibodies, which indicates the role of N1-type neutrophils in cancer immunotherapy. We also demonstrated that the anti-tumor activities of C/H treatment were enhanced by the administration of anti-PD-1 antibodies through neutrophil-mediated cytotoxic T lymphocyte activation. Thus, the triple combination of C/H and anti-PD-1 antibody C/H treatment may provide an improvement in cancer immunotherapy.

摘要

乳腺癌具有较高的转移风险；然而，尚未建立有效的治疗方法。我们开发了一种针对乳腺癌的新型免疫疗法，利用具有抗肿瘤特性的N1型中性粒细胞增强针对癌细胞的细胞毒性T淋巴细胞。为此，我们将CXCL2（CXC趋化因子配体2）质粒DNA与灭活的仙台病毒（日本血凝病毒）包膜（HVJ-E）相结合。CXCL2 DNA与HVJ-E的组合（C/H）通过增强细胞毒性T淋巴细胞抑制了原位同基因模型中小鼠乳腺癌的生长，并抑制了乳腺癌从原发灶向肺部的转移。经C/H处理后，肿瘤微环境中的N1型中性粒细胞（CD11b Ly6G FAS）增多，在给予抗中性粒细胞抗体后，C/H的肿瘤抑制作用和细胞毒性T淋巴细胞激活被阻断，这表明N1型中性粒细胞在癌症免疫治疗中的作用。我们还证明，通过中性粒细胞介导的细胞毒性T淋巴细胞激活，给予抗PD-1抗体可增强C/H治疗的抗肿瘤活性。因此，C/H与抗PD-1抗体的三联组合治疗可能会改善癌症免疫治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/fe947de4402f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/574aee83270c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/f947267dafd4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/7c2f50366e2e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/f26b03474a16/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/7077c1c9f120/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/0254817c90f7/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/fe947de4402f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/574aee83270c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/f947267dafd4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/7c2f50366e2e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/f26b03474a16/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/7077c1c9f120/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/0254817c90f7/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ae/7851488/fe947de4402f/gr6.jpg

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