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10.1038/ni.3269 http://scihub22266oqcxt.onion/10.1038/ni.3269 C4868085!4868085 !26414764     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26414764 &cmd=llinks): Failed to open stream: HTTP request failed! 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Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants |pdf=|usr=}}{{26414764 }} gab.com Text Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26414764 #FOAvip Human regulatory T cells (T(reg) cells) that develop from conventional T cells (T(conv) cells) following suboptimal stimulation via the T cell antigen receptor (TCR) (induced T(reg) cells (iT(reg) cells)) express the transcription factor Foxp3, are suppressive, and display an active proliferative and metabolic state. Here we found that the induction and suppressive function of iT(reg) cells tightly depended on glycolysis, which controlled Foxp3 splicing variants containing exon 2 (Foxp3-E2) through the glycolytic enzyme enolase-1. The Foxp3-E2-related suppressive activity of iT(reg) cells was altered in human autoimmune diseases, including multiple sclerosis and type 1 diabetes, and was associated with impaired glycolysis and signaling via interleukin 2. This link between glycolysis and Foxp3-E2 variants via enolase-1 shows a previously unknown mechanism for controlling the induction and function of T(reg) cells in health and in autoimmunity. Twit Text FOAVip Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26414764 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26414764 #FOAvip English Wikipedia <ref>{{Cite pmid|26414764 }}</ref> Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants #MMPMID26414764 De Rosa V ; Galgani M ; Porcellini A ; Colamatteo A ; Santopaolo M ; Zuchegna C ; Romano A ; De Simone S ; Procaccini C ; La Rocca C ; Carrieri PB ; Maniscalco GT ; Salvetti M ; Buscarinu MC ; Franzese A ; Mozzillo E ; La Cava A ; Matarese G Nat Immunol 2015[Nov]; 16 (11 ): 1174-84 PMID26414764 show ga Human regulatory T cells (T(reg) cells) that develop from conventional T cells (T(conv) cells) following suboptimal stimulation via the T cell antigen receptor (TCR) (induced T(reg) cells (iT(reg) cells)) express the transcription factor Foxp3, are suppressive, and display an active proliferative and metabolic state. Here we found that the induction and suppressive function of iT(reg) cells tightly depended on glycolysis, which controlled Foxp3 splicing variants containing exon 2 (Foxp3-E2) through the glycolytic enzyme enolase-1. The Foxp3-E2-related suppressive activity of iT(reg) cells was altered in human autoimmune diseases, including multiple sclerosis and type 1 diabetes, and was associated with impaired glycolysis and signaling via interleukin 2. This link between glycolysis and Foxp3-E2 variants via enolase-1 shows a previously unknown mechanism for controlling the induction and function of T(reg) cells in health and in autoimmunity. |Adult [MESH] |Alternative Splicing [MESH] |Autoimmunity [MESH] |Biomarkers, Tumor/antagonists & inhibitors/genetics/metabolism [MESH] |CD4-Positive T-Lymphocytes/classification/immunology/metabolism [MESH] |Case-Control Studies [MESH] |DNA-Binding Proteins/antagonists & inhibitors/genetics/metabolism [MESH] |Exons [MESH] |Fatty Acids/metabolism [MESH] |Female [MESH] |Forkhead Transcription Factors/antagonists & inhibitors/*genetics/metabolism [MESH] |Gene Knockdown Techniques [MESH] |Genetic Variation [MESH] |Glycolysis/*genetics [MESH] |Humans [MESH] |In Vitro Techniques [MESH] |Male [MESH] |Metabolome [MESH] |Middle Aged [MESH] |Multiple Sclerosis, Relapsing-Remitting/genetics/immunology/metabolism [MESH] |Oxidation-Reduction [MESH] |Phosphopyruvate Hydratase/antagonists & inhibitors/genetics/metabolism [MESH] |RNA, Messenger/genetics/metabolism [MESH] |Receptors, Antigen, T-Cell/metabolism [MESH] |Signal Transduction/immunology [MESH] |T-Lymphocytes, Regulatory/classification/*immunology/*metabolism [MESH] |Tumor Suppressor Proteins/antagonists & inhibitors/genetics/metabolism [MESH]Glycolysis controls the induction of human regulatory T cells by modul(epmc).pdf DeepDyve Pubget Overpricing