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10.1038/s41598-017-00235-3 http://scihub22266oqcxt.onion/10.1038/s41598-017-00235-3 C5428046!5428046!28273946     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 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28273946|t=2017. Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid |pdf=|usr=}}{{28273946}} gab.com Text Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28273946 #FOAvip Bullous pemphigoid (BP) is an autoimmune bullous disease caused by autoantibodies against BP180 in the epidermal basement membrane. Autoantibody-mediated complement activation is an important process in BP pathogenesis. CD46, a crucial complement regulatory protein in the complement activation, has been reported to be involved in several autoimmune diseases. In the present study, we investigated whether CD46 plays a role in BP development. We found that sCD46 expression was significantly increased in the serum and blister fluids of BP patients and correlated with the levels of anti-BP180 NC16A antibody and C3a. Otherwise, the level of mCD46 was decreased in lesions of BP patients, whereas the complement activation was enhanced. We also found that CD46 knockdown in HaCaT human keratinocytes enhanced autoantibody-mediated complement activation. Importantly, exogenous CD46 blocked complement activation in both healthy skin sections and keratinocytes induced by exposure to pathogenic antibodies from BP patients. These data suggest that CD46 deficiency is an important factor in BP pathogenesis and that increasing CD46 levels might be an effective treatment for BP. Twit Text FOAVip Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28273946 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28273946 #FOAvip English Wikipedia <ref>{{Cite pmid|28273946}}</ref> Dysregulation of mCD46 and sCD46 contribute to the pathogenesis of bullous pemphigoid #MMPMID28273946 Qiao P; Dang E; Cao T; Fang H; Zhang J; Qiao H; Wang G Sci Rep 2017[]; 7 (ä): ä PMID28273946show ga Bullous pemphigoid (BP) is an autoimmune bullous disease caused by autoantibodies against BP180 in the epidermal basement membrane. Autoantibody-mediated complement activation is an important process in BP pathogenesis. CD46, a crucial complement regulatory protein in the complement activation, has been reported to be involved in several autoimmune diseases. In the present study, we investigated whether CD46 plays a role in BP development. We found that sCD46 expression was significantly increased in the serum and blister fluids of BP patients and correlated with the levels of anti-BP180 NC16A antibody and C3a. Otherwise, the level of mCD46 was decreased in lesions of BP patients, whereas the complement activation was enhanced. We also found that CD46 knockdown in HaCaT human keratinocytes enhanced autoantibody-mediated complement activation. Importantly, exogenous CD46 blocked complement activation in both healthy skin sections and keratinocytes induced by exposure to pathogenic antibodies from BP patients. These data suggest that CD46 deficiency is an important factor in BP pathogenesis and that increasing CD46 levels might be an effective treatment for BP. äDysregulation of mCD46 and sCD46 contribute to the pathogenesis of bul(epmc).pdf DeepDyve Pubget Overpricing