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10.1146/annurev-pathol-011811-132453 http://scihub22266oqcxt.onion/10.1146/annurev-pathol-011811-132453 C5507606!5507606!23347350     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Annu+Rev+Pathol 2013 ; 8 (ä): 139-60 Nephropedia Template TP {{tp|p=23347350|t=2013. Pathogenesis of Antineutrophil Cytoplasmic Autoantibody?Associated Small-Vessel Vasculitis |pdf=|usr=}}{{23347350}} gab.com Text Pathogenesis of Antineutrophil Cytoplasmic Autoantibody Associated Small-Vessel Vasculitis JO: Annu Rev Pathol http://www.kidney.de/pget.php?&tw=1&pmid=23347350 #FOAvip Clinical, in vitro, and experimental animal observations indicate that antineutrophil cytoplasmic autoantibodies (ANCA) are pathogenic. The genesis of the ANCA autoimmune response is a multifactorial process that includes genetic predisposition, environmental adjuvant factors, an initiating antigen, and failure of T cell regulation. ANCA activate primed neutrophils (and monocytes) by binding to certain antigens expressed on the surface of neutrophils in specific inflammatory microenvironments. ANCA-activated neutrophils activate the alternative complement pathway, establishing an inflammatory amplification loop. The acute injury elicits an innate inflammatory response that recruits monocytes and T lymphocytes, which replace the neutrophils that have undergone karyorrhexis during acute inflammation. Extravascular granulomatous inflammation may be initiated by ANCA-induced activation of extravascular neutrophils, causing tissue necrosis and fibrin formation, which would elicit an influx of monocytes that transform into macrophages and multinucleated giant cells. Over time, the neutrophil-rich acute necrotizing lesions cause the accumulation of more lymphocytes, monocytes, and macrophages and produce typical granulomatous inflammation. Twit Text FOAVip Pathogenesis of Antineutrophil Cytoplasmic Autoantibody Associated Small-Vessel Vasculitis ????Annu Rev Pathol http://www.kidney.de/pget.php?&tw=1&pmid=23347350 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23347350 #FOAvip English Wikipedia <ref>{{Cite pmid|23347350}}</ref> Pathogenesis of Antineutrophil Cytoplasmic Autoantibody?Associated Small-Vessel Vasculitis #MMPMID23347350 Jennette JC; Falk RJ; Hu P; Xiao H Annu Rev Pathol 2013[Jan]; 8 (ä): 139-60 PMID23347350show ga Clinical, in vitro, and experimental animal observations indicate that antineutrophil cytoplasmic autoantibodies (ANCA) are pathogenic. The genesis of the ANCA autoimmune response is a multifactorial process that includes genetic predisposition, environmental adjuvant factors, an initiating antigen, and failure of T cell regulation. ANCA activate primed neutrophils (and monocytes) by binding to certain antigens expressed on the surface of neutrophils in specific inflammatory microenvironments. ANCA-activated neutrophils activate the alternative complement pathway, establishing an inflammatory amplification loop. The acute injury elicits an innate inflammatory response that recruits monocytes and T lymphocytes, which replace the neutrophils that have undergone karyorrhexis during acute inflammation. Extravascular granulomatous inflammation may be initiated by ANCA-induced activation of extravascular neutrophils, causing tissue necrosis and fibrin formation, which would elicit an influx of monocytes that transform into macrophages and multinucleated giant cells. Over time, the neutrophil-rich acute necrotizing lesions cause the accumulation of more lymphocytes, monocytes, and macrophages and produce typical granulomatous inflammation. äPathogenesis of Antineutrophil Cytoplasmic Autoantibody?Associated Sma(epmc).pdf DeepDyve Pubget Overpricing