巨噬细胞通过 TNF 信号直接杀死膀胱癌细胞,这是卡介苗疗法的早期反应。

IF 4 3区 医学 Q2 CELL BIOLOGY Disease Models & Mechanisms Pub Date : 2024-08-01 Epub Date: 2024-08-08 DOI:10.1242/dmm.050693
Mayra Fernanda Martínez-López, Cátia Rebelo de Almeida, Márcia Fontes, Raquel Valente Mendes, Stefan H E Kaufmann, Rita Fior
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引用次数: 0

摘要

卡介苗(BCG)是历史最悠久的癌症免疫治疗药物。尽管它很有效,但其最初的作用机制在很大程度上仍不为人所知。在这里,我们阐明了卡介苗诱导肿瘤清除的最早细胞机制。我们开发了一种快速的临床前体内试验,利用斑马鱼异种移植模型以单细胞分辨率实时观察膀胱癌细胞、卡介苗和先天性免疫之间最初的相互作用。我们的研究表明,卡介苗诱导巨噬细胞的募集和极化,使其趋向于促炎表型,同时诱导肿瘤微环境中的炎性细胞因子 tnfa、il1b 和 il6。巨噬细胞通过斑马鱼 TNF 信号直接诱导人类癌细胞凋亡。巨噬细胞对这一反应至关重要,因为巨噬细胞的耗竭会彻底消除卡介苗诱导的表型。与巨噬细胞的抗肿瘤活动主要依赖于刺激有效的适应性反应这一普遍概念相反,我们证明巨噬细胞本身就能诱导肿瘤凋亡和清除。因此,我们的研究结果揭示了卡介苗诱导的肿瘤免疫模型的另一个步骤,同时提供了概念验证实验,证明这种独特的模型具有测试先天免疫调节剂的潜力。
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Macrophages directly kill bladder cancer cells through TNF signaling as an early response to BCG therapy.

The Bacillus Calmette-Guérin (BCG) vaccine is the oldest cancer immunotherapeutic agent in use. Despite its effectiveness, its initial mechanisms of action remain largely unknown. Here, we elucidate the earliest cellular mechanisms involved in BCG-induced tumor clearance. We developed a fast preclinical in vivo assay to visualize in real time and at single-cell resolution the initial interactions among bladder cancer cells, BCG and innate immunity using the zebrafish xenograft model. We show that BCG induced the recruitment and polarization of macrophages towards a pro-inflammatory phenotype, accompanied by induction of the inflammatory cytokines tnfa, il1b and il6 in the tumor microenvironment. Macrophages directly induced apoptosis of human cancer cells through zebrafish TNF signaling. Macrophages were crucial for this response as their depletion completely abrogated the BCG-induced phenotype. Contrary to the general concept that macrophage anti-tumoral activities mostly rely on stimulating an effective adaptive response, we demonstrate that macrophages alone can induce tumor apoptosis and clearance. Thus, our results revealed an additional step to the BCG-induced tumor immunity model, while providing proof-of-concept experiments demonstrating the potential of this unique model to test innate immunomodulators.

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来源期刊
Disease Models & Mechanisms
Disease Models & Mechanisms 医学-病理学
CiteScore
6.60
自引率
7.00%
发文量
203
审稿时长
6-12 weeks
期刊介绍: Disease Models & Mechanisms (DMM) is an online Open Access journal focusing on the use of model systems to better understand, diagnose and treat human disease.
期刊最新文献
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