Inflammasomes in carcinogenesis and anticancer immune responses

被引:406
作者
Zitvogel, Laurence [1 ,2 ,3 ]
Kepp, Oliver [3 ,4 ]
Galluzzi, Lorenzo [3 ,4 ]
Kroemer, Guido [1 ,4 ,5 ,6 ,7 ]
机构
[1] Inst Gustave Roussy, Ctr Clin Invest CBT507, Villejuif, France
[2] INSERM, U1015, Villejuif, France
[3] Univ Paris 11, Villejuif, France
[4] INSERM, U848, Villejuif, France
[5] Ctr Rech Cordeliers, Paris, France
[6] Hop Europeen Georges Pompidou, AP HP, Paris, France
[7] Univ Paris 05, Paris, France
关键词
RECEPTOR ANTAGONIST ANAKINRA; CELL-DEATH; NLRP3; INFLAMMASOME; CROHNS-DISEASE; ADAPTIVE IMMUNITY; SUPPRESSOR-CELLS; INNATE IMMUNITY; PROTECTS MICE; IFN-GAMMA; CANCER;
D O I
10.1038/ni.2224
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
In the complex interplay between malignant cells and their microenvironment, caspase-1 activation complexes (inflammasomes) have contrasting roles. Inflammasomes may operate at the cell-autonomous level to eliminate malignant precursors through programmed cell death or, conversely, may stimulate the production of trophic factors for cancer cells and their stroma. In inflammatory cells, caspase-1 activation can fuel a cycle that leads to sterile inflammation and carcinogenesis, whereas in antigen-presenting cells, inflammasomes can stimulate anticancer immune responses. The inhibition of inflammasomes or neutralization of their products, mainly interleukin 1 beta (IL-1 beta) and IL-18, has profound effects on carcinogenesis and tumor progression. Thus, inflammasomes are promising therapeutic targets in cancer-related clinical conditions. Here we discuss present and future indications for the clinical use of inflammasome inhibitors.
引用
收藏
页码:343 / 351
页数:9
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