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10.1172/jci.insight.90111 http://scihub22266oqcxt.onion/10.1172/jci.insight.90111 C5374071!5374071 !28405610     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28405610 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       JCI+Insight 2017 ; 2 (7 ): e90111 Nephropedia Template TP {{tp|p=28405610 |t=2017. Btk-specific inhibition blocks pathogenic plasma cell signatures and myeloid cell-associated damage in IFN?-driven lupus nephritis |pdf=|usr=}}{{28405610 }} gab.com Text Btk-specific inhibition blocks pathogenic plasma cell signatures and myeloid cell-associated damage in IFN -driven lupus nephritis JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405610 #FOAvip Systemic lupus erythematosus (SLE) is often associated with exaggerated B cell activation promoting plasma cell generation, immune-complex deposition in the kidney, renal infiltration of myeloid cells, and glomerular nephritis. Type-I IFNs amplify these autoimmune processes and promote severe disease. Bruton's tyrosine kinase (Btk) inhibitors are considered novel therapies for SLE. We describe the characterization of a highly selective reversible Btk inhibitor, G-744. G-744 is efficacious, and superior to blocking BAFF and Syk, in ameliorating severe lupus nephritis in both spontaneous and IFN?-accelerated lupus in NZB/W_F1 mice in therapeutic regimens. Selective Btk inhibition ablated plasmablast generation, reduced autoantibodies, and - similar to cyclophosphamide - improved renal pathology in IFN?-accelerated lupus. Employing global transcriptional profiling of spleen and kidney coupled with cross-species human modular repertoire analyses, we identify similarities in the inflammatory process between mice and humans, and we demonstrate that G-744 reduced gene expression signatures essential for splenic B cell terminal differentiation, particularly the secretory pathway, as well as renal transcriptional profiles coupled with myeloid cell-mediated pathology and glomerular plus tubulointerstitial disease in human glomerulonephritis patients. These findings reveal the mechanism through which a selective Btk inhibitor blocks murine autoimmune kidney disease, highlighting pathway activity that may translate to human SLE. Twit Text FOAVip Btk-specific inhibition blocks pathogenic plasma cell signatures and myeloid cell-associated damage in IFN -driven lupus nephritis ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405610 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28405610 #FOAvip English Wikipedia <ref>{{Cite pmid|28405610 }}</ref> Btk-specific inhibition blocks pathogenic plasma cell signatures and myeloid cell-associated damage in IFN?-driven lupus nephritis #MMPMID28405610 Katewa A ; Wang Y ; Hackney JA ; Huang T ; Suto E ; Ramamoorthi N ; Austin CD ; Bremer M ; Chen JZ ; Crawford JJ ; Currie KS ; Blomgren P ; DeVoss J ; DiPaolo JA ; Hau J ; Johnson A ; Lesch J ; DeForge LE ; Lin Z ; Liimatta M ; Lubach JW ; McVay S ; Modrusan Z ; Nguyen A ; Poon C ; Wang J ; Liu L ; Lee WP ; Wong H ; Young WB ; Townsend MJ ; Reif K JCI Insight 2017[Apr]; 2 (7 ): e90111 PMID28405610 show ga Systemic lupus erythematosus (SLE) is often associated with exaggerated B cell activation promoting plasma cell generation, immune-complex deposition in the kidney, renal infiltration of myeloid cells, and glomerular nephritis. Type-I IFNs amplify these autoimmune processes and promote severe disease. Bruton's tyrosine kinase (Btk) inhibitors are considered novel therapies for SLE. We describe the characterization of a highly selective reversible Btk inhibitor, G-744. G-744 is efficacious, and superior to blocking BAFF and Syk, in ameliorating severe lupus nephritis in both spontaneous and IFN?-accelerated lupus in NZB/W_F1 mice in therapeutic regimens. Selective Btk inhibition ablated plasmablast generation, reduced autoantibodies, and - similar to cyclophosphamide - improved renal pathology in IFN?-accelerated lupus. Employing global transcriptional profiling of spleen and kidney coupled with cross-species human modular repertoire analyses, we identify similarities in the inflammatory process between mice and humans, and we demonstrate that G-744 reduced gene expression signatures essential for splenic B cell terminal differentiation, particularly the secretory pathway, as well as renal transcriptional profiles coupled with myeloid cell-mediated pathology and glomerular plus tubulointerstitial disease in human glomerulonephritis patients. These findings reveal the mechanism through which a selective Btk inhibitor blocks murine autoimmune kidney disease, highlighting pathway activity that may translate to human SLE. |Agammaglobulinaemia Tyrosine Kinase/*antagonists & inhibitors/metabolism [MESH] |Animals [MESH] |Autoantibodies/immunology [MESH] |B-Lymphocytes/drug effects/*immunology [MESH] |Cell Proliferation/drug effects [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Gene Expression/drug effects [MESH] |Humans [MESH] |Interferon-alpha/immunology [MESH] |Kidney/immunology/pathology [MESH] |Lupus Nephritis/*immunology/metabolism [MESH] |Lymphocyte Activation/drug effects [MESH] |Mice [MESH] |Mice, Inbred NZB [MESH] |Myeloid Cells/*metabolism [MESH]Btk-specific inhibition blocks pathogenic plasma cell signatures and m(epmc).pdf DeepDyve Pubget Overpricing