Signaling via MYD88 in the pancreatic tumor microenvironment A double-edged sword

被引：14
|
作者：
Zambirinis, Constantinos P. [1 ]
Miller, George [1 ,2 ]
机构：
[1] NYU, Dept Surg, S Arthur Localio Lab, Sch Med, New York, NY 10016 USA
[2] NYU, Sch Med, Dept Cell Biol, New York, NY 10016 USA
来源：
ONCOIMMUNOLOGY | 2013年 / 2卷 / 01期
关键词：
cancer-associated inflammation; dendritic cells; innate immunity; MYD88; pancreatic cancer; pattern-recognition receptors; Toll-like receptors; tumor microenvironment; NEGATIVE REGULATION;
D O I：
10.4161/onci.22567
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
We have recently shown that Toll-like receptor (TLR) signaling exacerbates pancreatic fibro-inflammation and promotes carcinogenesis in mice. Paradoxically, inhibition of the TLR-MYD88 signaling pathway is pro-tumorigenic owing to the dendritic cell-mediated T(H)2-polarization of CD4(+) T cells. TLR signaling appears to be central in pancreatic cancer-associated inflammation.
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页数：3
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