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10.1007/s10753-016-0351-1 http://scihub22266oqcxt.onion/10.1007/s10753-016-0351-1 C4883274!4883274!27083877     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Inflammation 2016 ; 39 (ä): 1169-76 Nephropedia Template TP {{tp|p=27083877|t=2016. Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis |pdf=|usr=}}{{27083877}} gab.com Text Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis JO: Inflammation http://www.kidney.de/pget.php?&tw=1&pmid=27083877 #FOAvip CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis. Twit Text FOAVip Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis ????Inflammation http://www.kidney.de/pget.php?&tw=1&pmid=27083877 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27083877 #FOAvip English Wikipedia <ref>{{Cite pmid|27083877}}</ref> Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis #MMPMID27083877 Du Y; Wu T; Zhou XJ; Davis LS; Mohan C Inflammation 2016[]; 39 (ä): 1169-76 PMID27083877show ga CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis. äBlockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis (epmc).pdf DeepDyve Pubget Overpricing