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关于“溶瘤腺病毒靶向释放双特异性融合蛋白SIRPα/Siglec-10可恢复肿瘤相关巨噬细胞活力以改善实体瘤治疗效果”的评论

Commentary on "Targeted release of a bispecific fusion protein SIRPα/Siglec-10 by oncolytic adenovirus reinvigorates tumor-associated macrophages to improve therapeutic outcomes in solid tumors".

作者信息

Lecoultre Marc, El Helali Aya

机构信息

Department of Medical Oncology and Hematology, University Hospital Zurich, Zürich, Switzerland.

Department of Clinical Oncology, Centre of Cancer Medicine, The University of Hong Kong, Hong Kong, Hong Kong

出版信息

J Immunother Cancer. 2025 Jun 15;13(6):e012218. doi: 10.1136/jitc-2025-012218.

Abstract

Tumor-associated macrophages (TAMs), long exploited by cancers to evade immune detection, can now be reprogrammed into potent antitumor effectors through cutting-edge viral engineering. In a landmark study published in the , Zhang introduced an innovative adenovirus, Adv-mSS, that blocks two critical "don't eat me" signals, CD47 and CD24, used by tumors to paralyze macrophage activity. By converting immunosuppressive TAMs into tumor-engulfing predators and reigniting CD8 T-cell response, Adv-mSS eradicated tumors across multiple preclinical models. This strategy offers a promising avenue for activating both innate and adaptive immunity against cancer and may address key limitations of current immunotherapies.

摘要

肿瘤相关巨噬细胞(TAM)长期以来被癌症利用以逃避免疫检测,如今通过前沿的病毒工程技术,可将其重新编程为强大的抗肿瘤效应细胞。在发表于[具体期刊名称未给出]的一项具有里程碑意义的研究中,张[具体姓名未给出]引入了一种创新型腺病毒Adv-mSS,它可阻断肿瘤用于麻痹巨噬细胞活性的两个关键“别吃我”信号,即CD47和CD24。通过将免疫抑制性TAM转化为吞噬肿瘤的“捕食者”并重新激发CD8 T细胞反应,Adv-mSS在多个临床前模型中根除了肿瘤。该策略为激活针对癌症的先天性和适应性免疫提供了一条有前景的途径,并且可能解决当前免疫疗法的关键局限性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d24/12314802/b701b6268d42/jitc-13-6-g001.jpg

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