Harnessing dendritic cells in cancer

被引：56

作者：

Apetoh, Lionel ^{[2
,3
,4
]}

Locher, Clara ^{[5
,6
]}

Ghiringhelli, Francois ^{[2
,3
,4
]}

Kroemer, Guido ^{[7
,8
,9
,10
]}

Zitvogel, Laurence ^{[1
,5
,6
]}

机构：

[1] Inst Gustave Roussy, Ctr Clin Invest Biotherapies, F-94805 Villejuif, France

[2] INSERM, U866, Dijon, France

[3] Univ Burgundy, Dijon, France

[4] Anticanc Ctr Georges Francois Leclerc, Dijon, France

[5] INSERM, U1015, Villejuif, France

[6] Univ Paris 11, Fac Paris Sud, Le Kremlin Bicetre, France

[7] INSERM, U848, Villejuif, France

[8] Ctr Rech Cordeliers, Paris, France

[9] Hop Europeen Georges Pompidou, AP HP, Paris, France

[10] Univ Paris 05, Paris, France

来源：

SEMINARS IN IMMUNOLOGY | 2011年 / 23卷 / 01期

关键词：

Dendritic cells; T-cells; Innate immunity; Adaptive immunity; Anticancer immunity; Immunomodulation; CD8(+) T-CELLS; IN-VIVO; ANTIGEN PRESENTATION; CROSS-PRESENTATION; IFN-GAMMA; ANTICANCER CHEMOTHERAPY; ADAPTIVE IMMUNITY; TUMOR-DEVELOPMENT; MELANOMA PATIENTS; SUPPRESSOR-CELLS;

D O I：

10.1016/j.smim.2011.01.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Dendritic cells (DCs) are central to the initiation of tumor-specific immune responses. However, the tumor microenvironment generates immunosuppressive cells and soluble mediators that compromise DC functions and limit the success of DC-based therapies. Progress in understanding DC metabolism in cancer is uncovering novel therapeutic targets that could restore DC capacity to prime T cells and trigger effective anticancer responses. Accumulating evidence also indicates that conventional chemo- and radiotherapy protocols can cause DC activation, enhance antigen cross-presentation, selectively eliminate immunosuppressive cells and revert the immunosuppression state caused by cancer, suggesting that relevant chemoimmunotherapy associations could fully exploit DC capacity to trigger anticancer responses. Here, we discuss recent strategies that harness DC against cancer. (C) 2011 Elsevier Ltd. All rights reserved.

引用

收藏

页码：42 / 49

页数：8

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