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10.4049/jimmunol.1303184 http://scihub22266oqcxt.onion/10.4049/jimmunol.1303184 C4130220!4130220!24879792     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 193 (1): 198-207 Nephropedia Template TP {{tp|p=24879792|t=2014. BCL6 Controls Th9 Cell Development by Repressing Il9 Transcription |pdf=|usr=}}{{24879792}} gab.com Text BCL6 Controls Th9 Cell Development by Repressing Il9 Transcription JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24879792 #FOAvip The transcriptional repressor B-cell lymphoma 6 (BCL6) is required for the development of T helper (Th) follicular cells and it has been shown to suppress Th2 cell differentiation. We demonstrate that BCL6 is a key regulator of Th9 cell development. BCL6 expression is transiently downregulated in polarized Th9 cells and forced expression of BCL6 in Th9 cells impairs Th9 cell differentiation. In contrast, BCL6 knockdown up-regulated interleukin (IL)-9 production in Th9 cells. The function of BCL6 in Th9 cells is under the control of IL-2/Janus kinase 3 (JAK3)/signal transducer and activator of transcription 5 (STAT5) signaling pathway. Using chromatin immunoprecipitation (ChIP), we show that in Th9 cells, BCL6 and STAT5 bind to adjacent motifs in the Il9 promoter. Furthermore, we found that STAT5 binding was associated with the abundance of a permissive histone mark at the Il9 promoter, while under conditions where BCL6 binding was predominant a repressive histone mark was prevalent. The effects of STAT5 and BCL6 on IL-9 transcription were further demonstrated using an IL-9-luciferase reporter assay where BCL6 repressed STAT5-mediated Il9 transactivation. In experimental autoimmune encephalomyelitis (EAE), forced expression of BCL6 in myelin oligodendrocyte glycoprotein (MOG)35?55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN? causing an exacerbation of the clinical disease. Our findings demonstrate a novel role of BCL6 in the regulation of Th9 cell development and their encephalitogenicity. Twit Text FOAVip BCL6 Controls Th9 Cell Development by Repressing Il9 Transcription ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24879792 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24879792 #FOAvip English Wikipedia <ref>{{Cite pmid|24879792}}</ref> BCL6 Controls Th9 Cell Development by Repressing Il9 Transcription #MMPMID24879792 Bassil R; Orent W; Olah M; Kurdi AT; Frangieh M; Buttrick T; Khoury SJ; Elyaman W J Immunol 2014[Jul]; 193 (1): 198-207 PMID24879792show ga The transcriptional repressor B-cell lymphoma 6 (BCL6) is required for the development of T helper (Th) follicular cells and it has been shown to suppress Th2 cell differentiation. We demonstrate that BCL6 is a key regulator of Th9 cell development. BCL6 expression is transiently downregulated in polarized Th9 cells and forced expression of BCL6 in Th9 cells impairs Th9 cell differentiation. In contrast, BCL6 knockdown up-regulated interleukin (IL)-9 production in Th9 cells. The function of BCL6 in Th9 cells is under the control of IL-2/Janus kinase 3 (JAK3)/signal transducer and activator of transcription 5 (STAT5) signaling pathway. Using chromatin immunoprecipitation (ChIP), we show that in Th9 cells, BCL6 and STAT5 bind to adjacent motifs in the Il9 promoter. Furthermore, we found that STAT5 binding was associated with the abundance of a permissive histone mark at the Il9 promoter, while under conditions where BCL6 binding was predominant a repressive histone mark was prevalent. The effects of STAT5 and BCL6 on IL-9 transcription were further demonstrated using an IL-9-luciferase reporter assay where BCL6 repressed STAT5-mediated Il9 transactivation. In experimental autoimmune encephalomyelitis (EAE), forced expression of BCL6 in myelin oligodendrocyte glycoprotein (MOG)35?55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN? causing an exacerbation of the clinical disease. Our findings demonstrate a novel role of BCL6 in the regulation of Th9 cell development and their encephalitogenicity. äBCL6 Controls Th9 Cell Development by Repressing Il9 Transcription (epmc).pdf DeepDyve Pubget Overpricing