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10.1038/s41598-018-25302-1 http://scihub22266oqcxt.onion/10.1038/s41598-018-25302-1 C5935736!5935736!29728568     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29728568|t=2018. Egr2-independent, Klf1-mediated induction of PD-L1 in CD4+ T cells |pdf=|usr=}}{{29728568}} gab.com Text Egr2-independent, Klf1-mediated induction of PD-L1 in CD4+ T cells JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29728568 #FOAvip Programmed death ligand 1 (PD-L1)-mediated induction of immune tolerance has been vigorously investigated in autoimmunity and anti-tumor immunity. However, details of the mechanism by which PD-L1 is induced in CD4+ T cells are unknown. Here, we revealed the potential function of Klf1 and Egr2-mediated induction of PD-L1 in CD4+ T cells. We focused on the molecules specifically expressed in CD4+CD25?LAG3+ regulatory T cells (LAG3+ Tregs) highly express of PD-L1 and transcription factor Egr2. Although ectopic expression of Egr2 induced PD-L1, a deficiency of Egr2 did not affect its expression, indicating the involvement of another PD-L1 induction mechanism. Comprehensive gene expression analysis of LAG3+ Tregs and in silico binding predictions revealed that Krüppel-like factor 1 (Klf1) is a candidate inducer of the PD-L1 gene (Cd274). Klf1 is a transcription factor that promotes ?-globin synthesis in erythroid progenitors, and its role in immunological homeostasis is unknown. Ectopic expression of Klf1 induced PD-L1 in CD4+ T cells through activation of the PI3K-mTOR signaling pathway, independent of STATs signaling and Egr2 expression. Our findings indicate that Klf1 and Egr2 are modulators of PD-L1-mediated immune suppression in CD4+ T cells and might provide new insights into therapeutic targets for autoimmune diseases and malignancies. Twit Text FOAVip Egr2-independent, Klf1-mediated induction of PD-L1 in CD4+ T cells ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29728568 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29728568 #FOAvip English Wikipedia <ref>{{Cite pmid|29728568}}</ref> Egr2-independent, Klf1-mediated induction of PD-L1 in CD4+ T cells #MMPMID29728568 Teruya S; Okamura T; Komai T; Inoue M; Iwasaki Y; Sumitomo S; Shoda H; Yamamoto K; Fujio K Sci Rep 2018[]; 8 (ä): ä PMID29728568show ga Programmed death ligand 1 (PD-L1)-mediated induction of immune tolerance has been vigorously investigated in autoimmunity and anti-tumor immunity. However, details of the mechanism by which PD-L1 is induced in CD4+ T cells are unknown. Here, we revealed the potential function of Klf1 and Egr2-mediated induction of PD-L1 in CD4+ T cells. We focused on the molecules specifically expressed in CD4+CD25?LAG3+ regulatory T cells (LAG3+ Tregs) highly express of PD-L1 and transcription factor Egr2. Although ectopic expression of Egr2 induced PD-L1, a deficiency of Egr2 did not affect its expression, indicating the involvement of another PD-L1 induction mechanism. Comprehensive gene expression analysis of LAG3+ Tregs and in silico binding predictions revealed that Krüppel-like factor 1 (Klf1) is a candidate inducer of the PD-L1 gene (Cd274). Klf1 is a transcription factor that promotes ?-globin synthesis in erythroid progenitors, and its role in immunological homeostasis is unknown. Ectopic expression of Klf1 induced PD-L1 in CD4+ T cells through activation of the PI3K-mTOR signaling pathway, independent of STATs signaling and Egr2 expression. Our findings indicate that Klf1 and Egr2 are modulators of PD-L1-mediated immune suppression in CD4+ T cells and might provide new insights into therapeutic targets for autoimmune diseases and malignancies. äEgr2-independent, Klf1-mediated induction of PD-L1 in CD4+ T cells (epmc).pdf DeepDyve Pubget Overpricing