化学
免疫系统
串扰
癌症研究
肿瘤微环境
CD8型
分泌物
细胞生物学
免疫学
生物
生物化学
物理
光学
作者
Junjie Qian,Limin Ding,Qinchuan Wu,Xiao Yu,Qiyong Li,Yangjun Gu,Shuai Wang,Jing Mao,Lifeng Xi,Bohan Li,Caixu Pan,Qianqian Wang,Yübo Wang,Liu Jianpeng,Yiting Qiao,Haiyang Xie,Tianchi Chen,Jiangzhen Ge,Lin Zhou,Shengyong Yin,Shusen Zheng
标识
DOI:10.1016/j.canlet.2023.216514
摘要
CD103+ DC is crucial for antitumor immune response. As a promising local therapy on cancers, nanosecond pulsed electric field (nsPEF) has been widely reported to stimulate anti-tumor immune response, but the underlying relationship between intratumoral CD103+ DC and nsPEF treatment remains enigmatic. Here, we focused on the behavior of CD103+ DC in response to nsPEF treatment and explored the underlying mechanism. We found that the nsPEF treatment led to the activation and accumulation of CD103+ DC in tumor. Depletion of CD103+ DC via Batf3-/- mice demonstrated CD103+ DC was necessary for intratumoral CD8+ T cell infiltration and activation in response to nsPEF treatment. Notably, NK cells recruited CD103+ DC into nsPEF-treated tumor through CCL5. Inflammatory array revealed CD103+ DC-derived IL-12 mediated the CCL5 secretion in NK cells. In addition, the boosted activation and infiltration of intratumoral CD103+ DC were abolished by cGAS-STING pathway inhibition, following IL-12 and CCL5 decreasing. Furthermore, nsPEF treatment promoting CD103+ DC-mediated antitumor response enhanced the effects of CD47 blockade strategy. Together, this study uncovers an unprecedented role for CD103+ DC in nsPEF treatment-elicited antitumor immune response and elucidates the underlying mechanisms.
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