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10.4049/jimmunol.1400614 http://scihub22266oqcxt.onion/10.4049/jimmunol.1400614 C4185231!4185231 !25210120     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25210120 &cmd=llinks): Failed to open stream: HTTP request failed! 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TLR2-dependent activation of ?-catenin pathway in dendritic cells induces regulatory responses and attenuates autoimmune inflammation |pdf=|usr=}}{{25210120 }} gab.com Text TLR2-dependent activation of -catenin pathway in dendritic cells induces regulatory responses and attenuates autoimmune inflammation JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25210120 #FOAvip Dendritic cells (DCs) sense microbes via multiple innate receptors. Signals from different innate receptors are coordinated and integrated by DCs to generate specific innate and adaptive immune responses against pathogens. Previously, we have shown that two pathogen recognition receptors, TLR2 and dectin-1, which recognize the same microbial stimulus (zymosan) on DCs, induce mutually antagonistic regulatory or inflammatory responses, respectively. How diametric signals from these two receptors are coordinated in DCs to regulate or incite immunity is not known. In this study, we show that TLR2 signaling via AKT activates the ?-catenin/T cell factor 4 pathway in DCs and programs them to drive T regulatory cell differentiation. Activation of ?-catenin/T cell factor 4 was critical to induce regulatory molecules IL-10 (Il-10) and vitamin A metabolizing enzyme retinaldehyde dehydrogenase 2 (Aldh1a2) and to suppress proinflammatory cytokines. Deletion of ?-catenin in DCs programmed them to drive Th17/Th1 cell differentiation in response to zymosan. Consistent with these findings, activation of the ?-catenin pathway in DCs suppressed chronic inflammation and protected mice from Th17/Th1-mediated autoimmune neuroinflammation. Thus, activation of ?-catenin in DCs via the TLR2 receptor is a novel mechanism in DCs that regulates autoimmune inflammation. Twit Text FOAVip TLR2-dependent activation of -catenin pathway in dendritic cells induces regulatory responses and attenuates autoimmune inflammation ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25210120 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25210120 #FOAvip English Wikipedia <ref>{{Cite pmid|25210120 }}</ref> TLR2-dependent activation of ?-catenin pathway in dendritic cells induces regulatory responses and attenuates autoimmune inflammation #MMPMID25210120 Manoharan I ; Hong Y ; Suryawanshi A ; Angus-Hill ML ; Sun Z ; Mellor AL ; Munn DH ; Manicassamy S J Immunol 2014[Oct]; 193 (8 ): 4203-13 PMID25210120 show ga Dendritic cells (DCs) sense microbes via multiple innate receptors. Signals from different innate receptors are coordinated and integrated by DCs to generate specific innate and adaptive immune responses against pathogens. Previously, we have shown that two pathogen recognition receptors, TLR2 and dectin-1, which recognize the same microbial stimulus (zymosan) on DCs, induce mutually antagonistic regulatory or inflammatory responses, respectively. How diametric signals from these two receptors are coordinated in DCs to regulate or incite immunity is not known. In this study, we show that TLR2 signaling via AKT activates the ?-catenin/T cell factor 4 pathway in DCs and programs them to drive T regulatory cell differentiation. Activation of ?-catenin/T cell factor 4 was critical to induce regulatory molecules IL-10 (Il-10) and vitamin A metabolizing enzyme retinaldehyde dehydrogenase 2 (Aldh1a2) and to suppress proinflammatory cytokines. Deletion of ?-catenin in DCs programmed them to drive Th17/Th1 cell differentiation in response to zymosan. Consistent with these findings, activation of the ?-catenin pathway in DCs suppressed chronic inflammation and protected mice from Th17/Th1-mediated autoimmune neuroinflammation. Thus, activation of ?-catenin in DCs via the TLR2 receptor is a novel mechanism in DCs that regulates autoimmune inflammation. |Adoptive Transfer [MESH] |Aldehyde Dehydrogenase 1 Family [MESH] |Aldehyde Dehydrogenase/biosynthesis [MESH] |Animals [MESH] |Autoimmunity/*immunology [MESH] |Cell Differentiation/immunology [MESH] |Dendritic Cells/*immunology [MESH] |Encephalomyelitis, Autoimmune, Experimental/chemically induced/immunology [MESH] |Inflammation/immunology/prevention & control [MESH] |Interleukin-10/biosynthesis [MESH] |Lectins, C-Type/immunology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Proto-Oncogene Proteins c-akt/immunology [MESH] |Retinal Dehydrogenase [MESH] |T-Lymphocytes, Regulatory/*cytology [MESH] |Th1 Cells/cytology/immunology [MESH] |Th17 Cells/cytology/immunology [MESH] |Toll-Like Receptor 2/*immunology [MESH] |Transcription Factor 7-Like 2 Protein/immunology [MESH] |Zymosan/immunology/pharmacology [MESH]TLR2-dependent activation of ?-catenin pathway in dendritic cells indu(epmc).pdf DeepDyve Pubget Overpricing