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10.4049/jimmunol.1601565 http://scihub22266oqcxt.onion/10.4049/jimmunol.1601565 C5360484!5360484!28219886     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2017 ; 198 (7): 2589-601 Nephropedia Template TP {{tp|p=28219886|t=2017. Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow-Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Micea |pdf=|usr=}}{{28219886}} gab.com Text Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow-Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Micea JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28219886 #FOAvip Glomerular damage mediated by glomerulus-infiltrating myeloid-derived cells is a key pathogenic event in lupus nephritis (LN)c but the process is poorly understood. Confocal microscopy of kidney sections and flow cytometry analysis of glomerular cells from magnetic-bead purified glomeruli have identified glomerulus-infiltrating leukocyte populations in NZM2328 (NZM) lupus-prone mice with spontaneous chronic glomerulonephritis (cGN) and anti-glomerular basement membrane (GBM)-induced nephritis. The occurrence of a major glomerulus-infiltrating CD11b+F4/80?I-A? macrophage population exhibiting the markers PD-L1, Mac-2, and macrophage mannose receptor (MMR, CD206) and producing Klf4, Il10, Retnla, Tnf, and Il6 mRNA which are known to be expressed by alternatively activated (M2b) macrophages correlated with proteinuria status. In NZM mice with spontaneous LN, glomerular macrophage infiltration is predominant. CD11b+F4/80?I-A? intraglomerular macrophages and PMN are important in inducing GN as anti- CD11b and ICAM-1 mAb inhibited both proteinuria and macrophage and PMN infiltration. The predominant and high expression of PD-L1 by CD11b+F4/80?I-A? glomerular macrophages in kidneys of mice with GN and the inhibition of proteinuria by anti-PD-L1 mAb supported the pathogenic role of these macrophages but not the PD-L1? PMN in GN development and in inducing podocyte damage. In NZM mice with spontaneous cGN and severe proteinuria, few glomerulus-infiltrating PMN were found, leaving macrophages and to a lesser extent DC as the major infiltrating leukocytes. These data taken together support the important pathogenic effect of CD11b+F4/80?I-A? M2b-like glomerulus-infiltrating macrophages in LN and reinforce macrophages as a promising target for GN treatment. Twit Text FOAVip Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow-Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Micea ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28219886 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28219886 #FOAvip English Wikipedia <ref>{{Cite pmid|28219886}}</ref> Dependence of Glomerulonephritis Induction on Novel Intraglomerular Alternatively Activated Bone Marrow-Derived Macrophages and Mac-1 and PD-L1 in Lupus-Prone NZM2328 Micea #MMPMID28219886 Sung SsJ; Ge Y; Dai C; Wang H; Fu SM; Sharma R; Hahn YS; Yu J; Le TH; Okusa MD; Bolton WK; Lawler JR J Immunol 2017[Apr]; 198 (7): 2589-601 PMID28219886show ga Glomerular damage mediated by glomerulus-infiltrating myeloid-derived cells is a key pathogenic event in lupus nephritis (LN)c but the process is poorly understood. Confocal microscopy of kidney sections and flow cytometry analysis of glomerular cells from magnetic-bead purified glomeruli have identified glomerulus-infiltrating leukocyte populations in NZM2328 (NZM) lupus-prone mice with spontaneous chronic glomerulonephritis (cGN) and anti-glomerular basement membrane (GBM)-induced nephritis. The occurrence of a major glomerulus-infiltrating CD11b+F4/80?I-A? macrophage population exhibiting the markers PD-L1, Mac-2, and macrophage mannose receptor (MMR, CD206) and producing Klf4, Il10, Retnla, Tnf, and Il6 mRNA which are known to be expressed by alternatively activated (M2b) macrophages correlated with proteinuria status. In NZM mice with spontaneous LN, glomerular macrophage infiltration is predominant. CD11b+F4/80?I-A? intraglomerular macrophages and PMN are important in inducing GN as anti- CD11b and ICAM-1 mAb inhibited both proteinuria and macrophage and PMN infiltration. The predominant and high expression of PD-L1 by CD11b+F4/80?I-A? glomerular macrophages in kidneys of mice with GN and the inhibition of proteinuria by anti-PD-L1 mAb supported the pathogenic role of these macrophages but not the PD-L1? PMN in GN development and in inducing podocyte damage. In NZM mice with spontaneous cGN and severe proteinuria, few glomerulus-infiltrating PMN were found, leaving macrophages and to a lesser extent DC as the major infiltrating leukocytes. These data taken together support the important pathogenic effect of CD11b+F4/80?I-A? M2b-like glomerulus-infiltrating macrophages in LN and reinforce macrophages as a promising target for GN treatment. äDependence of Glomerulonephritis Induction on Novel Intraglomerular Al(epmc).pdf DeepDyve Pubget Overpricing