原创力文档tgf-β suppresses β-catenin-dependent tolerogenic activation program in dendritic cellstgf-β抑制β-catenin-dependent耐受性树突状细胞激活项目.pdfVIP
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tgf-β suppresses β-catenin-dependent tolerogenic activation program in dendritic cellstgf-β抑制β-catenin-dependent耐受性树突状细胞激活项目
TGF-b Suppresses b-Catenin-Dependent Tolerogenic
Activation Program in Dendritic Cells
1 1 1 2,3 1 .
Bryan Vander Lugt , Zachary T. Beck , Robert C. Fuhlbrigge , Nir Hacohen , James J. Campbell * ,
1,4 .
Marianne Boes *
1 Department of Dermatology, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America, 2 Center for Immunology and Inflammatory Diseases,
Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Charlestown, Massachusetts, United States of America, 3 Broad Institute of Harvard
and MIT, Cambridge, Massachusetts, United States of America, 4 Division of Pediatric Immunology, University Medical Center Utrecht, Wilhelmina Children’s Hospital,
Utrecht, The Netherlands
Abstract
The mechanisms that underlie the critical dendritic cell (DC) function in maintainance of peripheral immune tolerance are
incompletely understood, although the b-catenin signaling pathway is critical for this role. The molecular details by which b-
catenin signaling is regulated in DCs are unknown. Mechanical disruption of murine bone marrow-derived DC (BMDC)
clusters activates DCs while maintaining their tolerogenic potential and this activation is associated with b-catenin signaling,
providing a useful model with which to explore tolerance-associated b-catenin signaling in DCs. In this report, we
demonstrate novel molecular features of the signaling events that control DC activation in response to mechanical
stimulation. Non-canonical b-catenin signaling is an essential component of this tolerogenic activation and is modulated by
adhesio
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