Immunogenic Cell Death in Cancer Therapy

被引:2459
|
作者
Kroemer, Guido [1 ,3 ,6 ,7 ,8 ,9 ]
Galluzzi, Lorenzo [5 ,8 ]
Kepp, Oliver [1 ,5 ,9 ]
Zitvogel, Laurence [2 ,4 ,9 ]
机构
[1] INSERM, U848, F-94805 Villejuif, France
[2] INSERM, U1015, F-94805 Villejuif, France
[3] Inst Gustave Roussy, Metab Platform, F-94805 Villejuif, France
[4] Inst Gustave Roussy, Ctr Clin Invest, F-94805 Villejuif, France
[5] Inst Gustave Roussy, F-94805 Villejuif, France
[6] Ctr Rech Cordeliers, Equipe Labellis Ligue Natl Canc 11, F-75006 Paris, France
[7] Hop Europeen Georges Pompidou, Pole Biol, AP HP, F-75015 Paris, France
[8] Univ Paris 05, Sorbonne Paris Cite, F-75006 Paris, France
[9] Univ Paris 11, F-94805 Villejuif, France
来源
关键词
ATP; autophagy; calreticulin; damage-associated molecular patterns; HMGB1; TLR4; ANTICANCER IMMUNE-RESPONSE; IN-SITU VACCINATION; FIND-ME SIGNAL; CALRETICULIN EXPOSURE; APOPTOTIC CELLS; TUMOR-CELLS; MOLECULAR-MECHANISMS; ADAPTIVE IMMUNITY; SURFACE EXPOSURE; T-CELLS;
D O I
10.1146/annurev-immunol-032712-100008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Depending on the initiating stimulus, cancer cell death can be immunogenic or nonimmunogenic. Immunogenic cell death (ICD) involves changes in the composition of the cell surface as well as the release of soluble mediators, occurring in a defined temporal sequence. Such signals operate on a series of receptors expressed by dendritic cells to stimulate the presentation of tumor antigens to T cells. We postulate that ICD constitutes a prominent pathway for the activation of the immune system against cancer, which in turn determines the long-term success of anticancer therapies. Hence, suboptimal regimens (failing to induce ICD), selective alterations in cancer cells (preventing the emission of immunogenic signals during ICD), or defects in immune effectors (abolishing the perception of ICD by the immune system) can all contribute to therapeutic failure. We surmise that ICD and its subversion by pathogens also play major roles in antiviral immune responses.
引用
收藏
页码:51 / 72
页数:22
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