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首页> 外文期刊>Antioxidants and redox signalling >Phototherapy-Induced Antitumor Immunity: Long-Term Tumor Suppression Effects via Photoinactivation of Respiratory Chain Oxidase-Triggered Superoxide Anion Burst
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Phototherapy-Induced Antitumor Immunity: Long-Term Tumor Suppression Effects via Photoinactivation of Respiratory Chain Oxidase-Triggered Superoxide Anion Burst

机译：光疗诱导的抗肿瘤免疫：通过呼吸链氧化酶触发的超氧阴离子爆裂的光灭活来长期抑制肿瘤。

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Aims: Our previous studies have demonstrated that as a mitochondria-targeting cancer phototherapy, high-fluence, low-power laser irradiation (HF-LPLI) results in oxidative damage that induces tumor cell apoptosis. In this study, we focused on the immunological effects of HF-LPLI phototherapy and explored its antitumor immune regulatory mechanism. Results: We found not only that HF-LPLI treatment induced tumor cell apoptosis but also that HF-LPLI-treated apoptotic tumor cells activated macrophages. Due to mitochondrial superoxide anion burst after HF-LPLI treatment, tumor cells displayed a high level of phosphatidylserine oxidation, which mediated the recognition and uptake by macrophages with the subsequent secretion of cytokines and generation of cytotoxic T lymphocytes. In addition, in vivo results showed that HF-LPLI treatment caused leukocyte infiltration into the tumor and efficaciously inhibited tumor growth in an EMT6 tumor model. These phenomena were absent in the respiration-deficient EMT6 tumor model, implying that the HF-LPLIelicited immunological effects were dependent on the mitochondrial superoxide anion burst. Innovation: In this study, for the first time, we show that HF-LPLI mediates tumor-killing effects via targeting photoinactivation of respiratory chain oxidase to trigger a superoxide anion burst, leading to a high level of oxidatively modified moieties, which contributes to the phenotypic changes in macrophages and mediates the antitumor immune response. Conclusion: Our results suggest that HF-LPLI may be an effective cancer treatment modality that both eradicates the treated primary tumors and induces an antitumor immune response via photoinactivation of respiratory chain oxidase to trigger superoxide anion burst.
机译：目的：我们以前的研究表明，作为靶向线粒体的癌症光疗，高通量，低功率激光照射（HF-LPLI）会导致氧化损伤，从而诱导肿瘤细胞凋亡。在这项研究中，我们集中于HF-LPLI光疗的免疫学作用，并探讨了其抗肿瘤免疫调节机制。结果：我们不仅发现HF-LPLI处理可诱导肿瘤细胞凋亡，而且还发现HF-LPLI处理的凋亡性肿瘤细胞可激活巨噬细胞。由于在HF-LPLI处理后线粒体超氧阴离子破裂，肿瘤细胞显示出高水平的磷脂酰丝氨酸氧化，其介导巨噬细胞的识别和摄取，随后分泌细胞因子并产生细胞毒性T淋巴细胞。另外，体内结果表明，在EMT6肿瘤模型中，HF-LPLI治疗引起白细胞浸润到肿瘤中并有效地抑制了肿瘤的生长。这些现象在呼吸不足的EMT6肿瘤模型中不存在，这表明HF-LPLI引起的免疫学效应取决于线粒体超氧阴离子的爆发。创新：在这项研究中，我们首次显示HF-LPLI通过靶向呼吸链氧化酶的光灭活以触发超氧阴离子爆发而介导肿瘤杀伤作用，从而导致高水平的氧化修饰部分，从而有助于巨噬细胞的表型变化并介导抗肿瘤免疫反应。结论：我们的结果表明，HF-LPLI可能是一种有效的癌症治疗方式，既可以根除已治疗的原发性肿瘤，又可以通过呼吸链氧化酶的光灭活引发超氧化物阴离子爆发而诱导抗肿瘤免疫反应。

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