免疫原性细胞死亡
免疫原性
钙网蛋白
依托泊苷
免疫系统
癌症研究
程序性细胞死亡
生物
丝裂霉素C
癌细胞
细胞凋亡
癌症
免疫学
免疫疗法
细胞生物学
化疗
生物化学
遗传学
内质网
作者
Michel Obéid,Antoine Tesnière,François Ghiringhelli,Gian María Fimia,Lionel Apétoh,Jean‐Luc Perfettini,Maria Castedo,Grégoire Mignot,Theocharis Panaretakis,Noëlia Casares,Didier Métivier,Nathanaël Larochette,Peter Van Endert,Fabiola Ciccosanti,Mauro Piacentini,Laurence Zitvogel,Guido Kroemer
出处
期刊:Nature Medicine
[Springer Nature]
日期:2006-12-24
卷期号:13 (1): 54-61
被引量:2786
摘要
Anthracyclin-treated tumor cells are particularly effective in eliciting an anticancer immune response, whereas other DNA-damaging agents such as etoposide and mitomycin C do not induce immunogenic cell death. Here we show that anthracyclins induce the rapid, preapoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knockdown of CRT suppressed the phagocytosis of anthracyclin-treated tumor cells by dendritic cells and abolished their immunogenicity in mice. The anthracyclin-induced CRT translocation was mimicked by inhibition of the protein phosphatase 1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase 1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anticancer immune responses and delineate a possible strategy for immunogenic chemotherapy.
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