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      Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine.

      Science (New York, N.Y.)

      Animals, Cytokines, metabolism, Dendritic Cells, immunology, Gene Expression Profiling, Inflammation, Inflammatory Bowel Diseases, Intestinal Mucosa, cytology, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oligonucleotide Array Sequence Analysis, Self Tolerance, Signal Transduction, T-Lymphocytes, Helper-Inducer, T-Lymphocytes, Regulatory, Tretinoin, Wnt Proteins, beta Catenin

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          Abstract

          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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          Author and article information

          Journal
          20705860
          3732486
          10.1126/science.1188510

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