Notch and Wingless Signaling Cooperate in Regulation of Dendritic Cell Differentiation

被引：100

作者：

Zhou, Jie ^{[1
]}

Cheng, Pingyan ^{[1
]}

Youn, Je-In ^{[1
]}

Cotter, Matthew J. ^{[1
]}

Gabrilovich, Dmitry I. ^{[1
,2
,3
]}

机构：

[1] Univ S Florida, H Lee Moffit Canc Ctr & Res Inst, Dept Immunol, Tampa, FL 33612 USA

[2] Univ S Florida, Dept Mol Med, Tampa, FL 33612 USA

[3] Univ S Florida, Dept Oncol Sci, Tampa, FL 33612 USA

来源：

IMMUNITY | 2009年 / 30卷 / 06期

关键词：

BONE-MARROW STROMA; BETA-CATENIN; LIGAND DELTA-1; T-CELLS; WNT; EXPRESSION; MONOCYTES; PATHWAY; LYMPHOPOIESIS; HEMATOPOIESIS;

D O I：

10.1016/j.immuni.2009.03.021

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Dendritic cell (DC) differentiation is regulated by stroma via a network of soluble and cell-bound factors. Notch is one of the major elements of this network. Its role in DC differentiation, however, is controversial. Here, we demonstrate that activation of Notch signaling in hematopoietic progenitor cells (HPCs) promoted differentiation of conventional DCs via activation of the canonical Wingless (Wnt) pathway. Inhibition of the Wnt pathway abrogated the effect of Notch on DC differentiation. The fact that activation of the Wnt pathway in Notch-1-deficient embryonic stem cells restored DC differentiation indicates that Wnt signaling is downstream of the Notch pathway in regulating DC differentiation. Notch signaling activated the Wnt pathway in HPCs via expression of multiple members of the Frizzled family of Wnt receptors, which was directly regulated by the CSL (RPB-J kappa) transcription factor. Thus, these data suggest a model of DC differentiation via cooperation between Wnt and Notch pathways.

引用

页码：845 / 859

页数：15

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