Tumor-Induced Disruption of Proximal TCR-Mediated Signal Transduction in Tumor-Infiltrating CD8+ Lymphocytes Inactivates Antitumor Effector Phase

被引:37
作者
Vazquez-Cintron, Edwin J. [1 ]
Monu, Ngozi R. [1 ,2 ]
Frey, Alan B. [1 ]
机构
[1] NYU, Langone Med Ctr, Dept Cell Biol, New York, NY 10016 USA
[2] NYU, Langone Med Ctr, New York Univ Canc Inst, New York, NY 10016 USA
基金
美国国家卫生研究院;
关键词
T-CELL-ACTIVATION; TRANSMEMBRANE ADAPTER PROTEIN; NATURAL-KILLER-CELLS; TYROSINE-PHOSPHATASE SHP-1; IMMATURE MYELOID CELLS; DENDRITIC CELLS; INHIBITORY RECEPTOR; IN-VIVO; TRYPTOPHAN CATABOLISM; IMMUNE-SYSTEM;
D O I
10.4049/jimmunol.1001157
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 presence in cancer tissue of Ag-specific, activated tumor infiltrating CD8(+) T cells proves that tumors express Ags capable of eliciting immune response. Therefore, in general, tumor escape from immune-mediated clearance is not attributable to immunological ignorance. However, tumor-infiltrating lymphocytes are defective in effector phase function, demonstrating tumor-induced immune suppression that likely underlies tumor escape. Since exocytosis of lytic granules is dependent upon TCR-mediated signal transduction, it is a reasonable contention that tumors may induce defective signal transduction in tumor infiltrating T cells. In this review, we consider the biochemical basis for antitumor T cell dysfunction, focusing on the role of inhibitory signaling receptors in restricting TCR-mediated signaling in tumor-infiltrating lymphocytes. The Journal of Immunology, 2010, 185: 7133-7140.
引用
收藏
页码:7133 / 7140
页数:8
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