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10.4049/jimmunol.1500418 http://scihub22266oqcxt.onion/10.4049/jimmunol.1500418 C4868781!4868781 !27059595     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27059595 &cmd=llinks): Failed to open stream: HTTP request failed! 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Apoptotic Debris Accumulates on Hematopoietic Cells and Promotes Disease in Murine and Human Systemic Lupus Erythematosus |pdf=|usr=}}{{27059595 }} gab.com Text Apoptotic Debris Accumulates on Hematopoietic Cells and Promotes Disease in Murine and Human Systemic Lupus Erythematosus 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 PBMCs 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 wk 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. Taken 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 Systemic Lupus Erythematosus ????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 Systemic Lupus Erythematosus #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 PMID27059595 show 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 PBMCs 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 wk 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. Taken together, our findings reveal a previously unappreciated role for the cell surface accumulation of IgG-ICs in human and murine lupus. |*Apoptosis [MESH] |Adult [MESH] |Animals [MESH] |Autoantigens/immunology/metabolism [MESH] |B-Cell Activating Factor/metabolism [MESH] |Blood Cells/*immunology [MESH] |Dendritic Cells/*immunology [MESH] |Female [MESH] |Humans [MESH] |Lupus Erythematosus, Systemic/*immunology [MESH] |Macrophages/*immunology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Inbred MRL lpr [MESH] |Mice, Knockout [MESH] |Middle Aged [MESH] |Receptors, IgG/genetics [MESH]Apoptotic Debris Accumulates on Hematopoietic Cells and Promotes Disea(epmc).pdf DeepDyve Pubget Overpricing