Journal
SCIENCE
Volume 329, Issue 5993, Pages 849-853Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1188510
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Funding
- National Institutes of Health [U54AI057157, R37AI48638, R01DK057665, U19AI057266, HHSN266 200700006C, NO1 AI50019, NO1 AI50025]
- Bill & Melinda Gates Foundation
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Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
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