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10.4049/jimmunol.1500418 http://scihub22266oqcxt.onion/10.4049/jimmunol.1500418 C4868781!4868781!27059595     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2016 ; 196 (10): 4030-9 Nephropedia Template TP {{tp|p=27059595|t=2016. Apoptotic debris accumulates on hematopoietic cells and promotes disease in murine and human SLE1 |pdf=|usr=}}{{27059595}} gab.com Text Apoptotic debris accumulates on hematopoietic cells and promotes disease in murine and human SLE1 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27059595 #FOAvip Apoptotic debris, autoantibody, and IgG-immune complexes (ICs) have long been implicated in the inflammation associated with systemic lupus erythematosus (SLE); however, it remains unclear whether they initiate immune-mediated events that promote disease. In this study, we show that peripheral blood mononuclear cells from SLE patients experiencing active disease, and hematopoietic cells from lupus-prone MRL/lpr and NZM2410 mice accumulate markedly elevated levels of surface-bound nuclear self-antigens. On dendritic cells (DCs) and macrophages (MFs), the self-antigens are part of IgG-ICs that promote Fc?RI-mediated signal transduction. Accumulation of IgG-ICs is evident on ex vivo myeloid cells from MRL/lpr mice by 10 weeks of age, and steadily increases prior to lupus nephritis. IgG and Fc?RI play a critical role in disease pathology. Passive transfer of pathogenic IgG into IgG-deficient MRL/lpr mice promotes the accumulation of IgG-ICs prior to significant B cell expansion, BAFF secretion, and lupus nephritis. In contrast, diminishing the burden IgG-ICs in MRL/lpr mice through deficiency in Fc?RI markedly improves these lupus pathologies. Together, our findings reveal a previously unappreciated role for the cell surface accumulation of IgG-ICs in human and murine lupus. Twit Text FOAVip Apoptotic debris accumulates on hematopoietic cells and promotes disease in murine and human SLE1 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27059595 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27059595 #FOAvip English Wikipedia <ref>{{Cite pmid|27059595}}</ref> Apoptotic debris accumulates on hematopoietic cells and promotes disease in murine and human SLE1 #MMPMID27059595 Kang S; Rogers JL; Monteith AJ; Jiang C; Schmitz J; Clarke SH; Tarrant TK; Truong YK; Diaz M; Fedoriw Y; Vilen BJ J Immunol 2016[May]; 196 (10): 4030-9 PMID27059595show ga Apoptotic debris, autoantibody, and IgG-immune complexes (ICs) have long been implicated in the inflammation associated with systemic lupus erythematosus (SLE); however, it remains unclear whether they initiate immune-mediated events that promote disease. In this study, we show that peripheral blood mononuclear cells from SLE patients experiencing active disease, and hematopoietic cells from lupus-prone MRL/lpr and NZM2410 mice accumulate markedly elevated levels of surface-bound nuclear self-antigens. On dendritic cells (DCs) and macrophages (MFs), the self-antigens are part of IgG-ICs that promote Fc?RI-mediated signal transduction. Accumulation of IgG-ICs is evident on ex vivo myeloid cells from MRL/lpr mice by 10 weeks of age, and steadily increases prior to lupus nephritis. IgG and Fc?RI play a critical role in disease pathology. Passive transfer of pathogenic IgG into IgG-deficient MRL/lpr mice promotes the accumulation of IgG-ICs prior to significant B cell expansion, BAFF secretion, and lupus nephritis. In contrast, diminishing the burden IgG-ICs in MRL/lpr mice through deficiency in Fc?RI markedly improves these lupus pathologies. Together, our findings reveal a previously unappreciated role for the cell surface accumulation of IgG-ICs in human and murine lupus. äApoptotic debris accumulates on hematopoietic cells and promotes disea(epmc).pdf DeepDyve Pubget Overpricing