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10.3389/fimmu.2017.01565 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.01565 29204146!5698275!29204146     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29204146&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Front+Immunol 2017 ; 8 (?): 1565 Nephropedia Template TP {{tp|p=29204146|t=2017. Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during Late Sepsis |pdf=|usr=}}{{29204146}} gab.com Text Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during Late Sepsis JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29204146 #FOAvip Myeloid precursor cell reprogramming into a myeloid-derived suppressor cell (MDSC) contributes to high mortality rates in mouse and human sepsis. S100A9 mRNA and intracellular protein levels increase during early sepsis and remain elevated in Gr1(+)CD11b(+) MDSCs after pro-inflammatory sepsis transitions to the later chronic anti-inflammatory and immunosuppressive phenotype. The purpose of this study was to determine whether intracellular S100A9 protein might sustain Gr1(+)CD11b(+) MDSC repressor cell reprogramming during sepsis. We used a chronic model of sepsis in mice to show that S100A9 release from MDSCs and circulating phagocytes decreases after early sepsis and that targeting the S100a9 gene improves survival. Surprisingly, we find that intracellular S100A9 protein translocates from the cytosol to nucleus in Gr1(+)CD11b(+) MDSCs during late sepsis and promotes expression of miR-21 and miR-181b immune repressor mediators. We further provide support of this immunosuppression pathway in human sepsis. This study may inform a new therapeutic target for improving sepsis outcome. Twit Text FOAVip Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during Late Sepsis ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29204146 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29204146 #FOAvip English Wikipedia <ref>{{Cite pmid|29204146}}</ref> Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during Late Sepsis #MMPMID29204146 Dai J; Kumbhare A; Youssef D; McCall CE; El Gazzar M Front Immunol 2017[]; 8 (?): 1565 PMID29204146show ga Myeloid precursor cell reprogramming into a myeloid-derived suppressor cell (MDSC) contributes to high mortality rates in mouse and human sepsis. S100A9 mRNA and intracellular protein levels increase during early sepsis and remain elevated in Gr1(+)CD11b(+) MDSCs after pro-inflammatory sepsis transitions to the later chronic anti-inflammatory and immunosuppressive phenotype. The purpose of this study was to determine whether intracellular S100A9 protein might sustain Gr1(+)CD11b(+) MDSC repressor cell reprogramming during sepsis. We used a chronic model of sepsis in mice to show that S100A9 release from MDSCs and circulating phagocytes decreases after early sepsis and that targeting the S100a9 gene improves survival. Surprisingly, we find that intracellular S100A9 protein translocates from the cytosol to nucleus in Gr1(+)CD11b(+) MDSCs during late sepsis and promotes expression of miR-21 and miR-181b immune repressor mediators. We further provide support of this immunosuppression pathway in human sepsis. This study may inform a new therapeutic target for improving sepsis outcome. ?Intracellular S100A9 Promotes Myeloid-Derived Suppressor Cells during (epmc).pdf DeepDyve Pubget Overpricing