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10.1038/ncomms14945 http://scihub22266oqcxt.onion/10.1038/ncomms14945 C5458132!5458132!28530237     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28530237|t=2017. Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity |pdf=|usr=}}{{28530237}} gab.com Text Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28530237 #FOAvip Antibodies recognizing complexes of the chemokine platelet factor 4 (PF4/CXCL4) and polyanions (P) opsonize PF4-coated bacteria hereby mediating bacterial host defense. A subset of these antibodies may activate platelets after binding to PF4/heparin complexes, causing the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). In autoimmune-HIT, anti-PF4/P-antibodies activate platelets in the absence of heparin. Here we show that antibodies with binding forces of approximately 60?100?pN activate platelets in the presence of polyanions, while a subset of antibodies from autoimmune-HIT patients with binding forces ?100?pN binds to PF4 alone in the absence of polyanions. These antibodies with high binding forces cluster PF4-molecules forming antigenic complexes which allow binding of polyanion-dependent anti-PF4/P-antibodies. The resulting immunocomplexes induce massive platelet activation in the absence of heparin. Antibody-mediated changes in endogenous proteins that trigger binding of otherwise non-pathogenic (or cofactor-dependent) antibodies may also be relevant in other antibody-mediated autoimmune disorders. Twit Text FOAVip Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28530237 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28530237 #FOAvip English Wikipedia <ref>{{Cite pmid|28530237}}</ref> Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity #MMPMID28530237 Nguyen TH; Medvedev N; Delcea M; Greinacher A Nat Commun 2017[]; 8 (ä): ä PMID28530237show ga Antibodies recognizing complexes of the chemokine platelet factor 4 (PF4/CXCL4) and polyanions (P) opsonize PF4-coated bacteria hereby mediating bacterial host defense. A subset of these antibodies may activate platelets after binding to PF4/heparin complexes, causing the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). In autoimmune-HIT, anti-PF4/P-antibodies activate platelets in the absence of heparin. Here we show that antibodies with binding forces of approximately 60?100?pN activate platelets in the presence of polyanions, while a subset of antibodies from autoimmune-HIT patients with binding forces ?100?pN binds to PF4 alone in the absence of polyanions. These antibodies with high binding forces cluster PF4-molecules forming antigenic complexes which allow binding of polyanion-dependent anti-PF4/P-antibodies. The resulting immunocomplexes induce massive platelet activation in the absence of heparin. Antibody-mediated changes in endogenous proteins that trigger binding of otherwise non-pathogenic (or cofactor-dependent) antibodies may also be relevant in other antibody-mediated autoimmune disorders. äAnti-platelet factor 4/polyanion antibodies mediate a new mechanism of(epmc).pdf DeepDyve Pubget Overpricing