Antitumor Immunity Induced after α Irradiation

免疫原性细胞死亡 免疫系统 癌症研究 免疫原性 获得性免疫系统 免疫 放射免疫疗法 放射生物学 生物 免疫学 免疫疗法 医学 放射治疗 抗体 单克隆抗体 内科学
作者
Jean‐Baptiste Gorin,Jérémie Ménager,Sébastien Gouard,Catherine Maurel,Yannick Guilloux,Alain Faivre-Chauvet,Aliyah Morgenstern,Frank Bruchertseifer,Michel Chérel,François Davodeau,Joëlle Gaschet
出处
期刊:Neoplasia [Elsevier BV]
卷期号:16 (4): 319-328 被引量:82
标识
DOI:10.1016/j.neo.2014.04.002
摘要

Radioimmunotherapy (RIT) is a therapeutic modality that allows delivering of ionizing radiation directly to targeted cancer cells. Conventional RIT uses β-emitting radioisotopes, but recently, a growing interest has emerged for the clinical development of α particles. α emitters are ideal for killing isolated or small clusters of tumor cells, thanks to their specific characteristics (high linear energy transfer and short path in the tissue), and their effect is less dependent on dose rate, tissue oxygenation, or cell cycle status than γ and X rays. Several studies have been performed to describe α emitter radiobiology and cell death mechanisms induced after α irradiation. But so far, no investigation has been undertaken to analyze the impact of α particles on the immune system, when several studies have shown that external irradiation, using γ and X rays, can foster an antitumor immune response. Therefore, we decided to evaluate the immunogenicity of murine adenocarcinoma MC-38 after bismuth-213 (213Bi) irradiation using a vaccination approach. In vivo studies performed in immunocompetent C57Bl/6 mice induced a protective antitumor response that is mediated by tumor-specific T cells. The molecular mechanisms potentially involved in the activation of adaptative immunity were also investigated by in vitro studies. We observed that 213Bi-treated MC-38 cells release "danger signals" and activate dendritic cells. Our results demonstrate that α irradiation can stimulate adaptive immunity, elicits an efficient antitumor protection, and therefore is an immunogenic cell death inducer, which provides an attractive complement to its direct cytolytic effect on tumor cells.
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