The dendritic cell-tumor cross-talk in cancer

被引:60
|
作者
Ma, Yuting [1 ,2 ]
Aymeric, Laetitia [1 ,2 ]
Locher, Clara [1 ,2 ]
Kroemer, Guido [3 ,5 ,6 ]
Zitvogel, Laurence [1 ,2 ,4 ,7 ]
机构
[1] Inst Gustave Roussy, INSERM, U1015, F-94805 Villejuif, France
[2] Univ Paris 11, F-94805 Villejuif, France
[3] INSERM, U848, Villejuif, France
[4] Ctr Rech Cordeliers, Paris, France
[5] Hop Europeen Georges Pompidou, AP HP, Paris, France
[6] Univ Paris 05, Paris 5, France
[7] Inst Gustave Roussy, CICBT507, F-94805 Villejuif, France
关键词
CD4(+) T-CELLS; APOPTOTIC CELLS; IN-VIVO; RECEPTOR; IMMUNITY; CALRETICULIN; THERAPY; ALPHA; SPHINGOSINE-1-PHOSPHATE; IDENTIFICATION;
D O I
10.1016/j.coi.2010.09.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The question as to whether the tumor grows because of or despite the host immune system is being progressively addressed with refined technology, gene targeting in mice and human translational research. The productive interplay between major actors of the antitumor immunity is actively compromised by the tumor microenvironment subverting the links between innate and cognate immunity and/or generating devastating new players. The complexity of the host tumor equilibrium could be dissected at the reduced level of the dialogue between professional antigen presenting cells (APC), more precisely dendritic cells, and tumor cells that may profoundly dictate the outcome of the neoplasma. This review will summarize the novel mechanisms by which tumor cells regulate DC recruitment, differentiation, activation and cross-presenting functions in tumor beds and how innate players might counterbalance these interactions. Finally, we will highlight interesting strategies that harness the DC potential to fight against cancer.
引用
收藏
页码:146 / 152
页数:7
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