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.

引用

页数：3

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