Macrophages eat cancer cells using their own calreticulin as a guide: Roles of TLR and Btk

被引：215

作者：

Feng, Mingye ^{[1
,2
,3
]}

Chen, James Y. ^{[1
,2
,3
]}

Weissman-Tsukamoto, Rachel ^{[1
,2
,3
]}

Volkmer, Jens-Peter ^{[1
,2
,3
]}

Ho, Po Yi ^{[1
,2
,3
]}

McKenna, Kelly M. ^{[1
,2
,3
]}

Cheshier, Samuel ^{[1
]}

Zhang, Michael ^{[1
]}

Guo, Nan ^{[1
,2
,3
]}

Gip, Phung ^{[1
,2
,3
]}

Mitra, Siddhartha S. ^{[1
]}

Weissman, Irving L. ^{[1
,2
,3
,4
]}

机构：

[1] Stanford Univ, Sch Med, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA

[2] Stanford Univ, Sch Med, Ludwig Ctr Canc Stem Cell Res & Med, Stanford, CA 94305 USA

[3] Stanford Univ, Sch Med, Stanford Canc Inst, Stanford, CA 94305 USA

[4] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2015年 / 112卷 / 07期

基金：

美国国家卫生研究院;

关键词：

immunosurveillance; programmed cell removal; Bruton's tyrosine kinase; eat me" signal; Toll-like receptor; BRUTONS TYROSINE KINASE; X-LINKED AGAMMAGLOBULINEMIA; PROMOTE PHAGOCYTOSIS; SURFACE CALRETICULIN; APOPTOTIC CELLS; STEM-CELLS; CD47; TARGET; CLEARANCE; PROTEIN;

D O I：

10.1073/pnas.1424907112

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Macrophage-mediated programmed cell removal (PrCR) is an important mechanism of eliminating diseased and damaged cells before programmed cell death. The induction of PrCR by eat-me signals on tumor cells is countered by don't-eat-me signals such as CD47, which binds macrophage signal-regulatory protein a to inhibit phagocytosis. Blockade of CD47 on tumor cells leads to phagocytosis by macrophages. Here we demonstrate that the activation of Toll-like receptor (TLR) signaling pathways in macrophages synergizes with blocking CD47 on tumor cells to enhance PrCR. Bruton's tyrosine kinase (Btk) mediates TLR signaling in macrophages. Calreticulin, previously shown to be an eat-me signal on cancer cells, is activated in macrophages for secretion and cell-surface exposure by TLR and Btk to target cancer cells for phagocytosis, even if the cancer cells themselves do not express calreticulin.

引用

页码：2145 / 2150

页数：6

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