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10.1016/j.autrev.2016.03.011 http://scihub22266oqcxt.onion/10.1016/j.autrev.2016.03.011 C4875785!4875785!26970483     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Autoimmun+Rev 2016 ; 15 (7): 752-5 Nephropedia Template TP {{tp|p=26970483|t=2016. Atomic features of an autoantigen in heparin-induced thrombocytopenia (HIT) |pdf=|usr=}}{{26970483}} gab.com Text Atomic features of an autoantigen in heparin-induced thrombocytopenia (HIT) JO: Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=26970483 #FOAvip Autoantigen development is poorly understood at the atomic level. Heparin-induced thrombocytopenia (HIT) is an autoimmune thrombotic disorder caused by antibodies to an antigen composed of platelet factor 4 (PF4) and heparin or cellular glycosaminoglycans (GAGs). In solution, PF4 exists as an equilibrium among monomers, dimers and tetramers. Structural studies of these interacting components helped delineate a multi-step process involved in the pathogenesis of HIT. First, heparin binds to the ?closed? end of the PF4 tetramer, and stabilizes its conformation and exposing the ?open? end. Second, PF4 arrays along heparin/GAG chains, which approximates tetramers, forming large antigenic complexes that enhance antibody avidity. Third, pathogenic HIT antibodies bind to the ?open? end of stabilized PF4 tetramers to form an IgG/PF4/heparin ternary immune complex and also to propagate formation of ?ultralarge immune complexes? (ULCs) that contain multiple IgG antibodies. Fourth, ULCs signal through Fc?RIIA receptors, activating platelets and monocytes directly and generating thrombin, which transactivates hematopoietic and endothelial cells. A non-pathogenic anti-PF4 antibody prevents tetramer formation, binding of pathogenic antibody, platelet activation and thrombosis, providing a new approach to manage HIT. An improved understanding of the pathogenesis of HIT may lead to novel diagnostics and therapeutics for this autoimmune disease. Twit Text FOAVip Atomic features of an autoantigen in heparin-induced thrombocytopenia (HIT) ????Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=26970483 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26970483 #FOAvip English Wikipedia <ref>{{Cite pmid|26970483}}</ref> Atomic features of an autoantigen in heparin-induced thrombocytopenia (HIT) #MMPMID26970483 Cai Z; Zhu Z; Greene MI; Cines DB Autoimmun Rev 2016[Jul]; 15 (7): 752-5 PMID26970483show ga Autoantigen development is poorly understood at the atomic level. Heparin-induced thrombocytopenia (HIT) is an autoimmune thrombotic disorder caused by antibodies to an antigen composed of platelet factor 4 (PF4) and heparin or cellular glycosaminoglycans (GAGs). In solution, PF4 exists as an equilibrium among monomers, dimers and tetramers. Structural studies of these interacting components helped delineate a multi-step process involved in the pathogenesis of HIT. First, heparin binds to the ?closed? end of the PF4 tetramer, and stabilizes its conformation and exposing the ?open? end. Second, PF4 arrays along heparin/GAG chains, which approximates tetramers, forming large antigenic complexes that enhance antibody avidity. Third, pathogenic HIT antibodies bind to the ?open? end of stabilized PF4 tetramers to form an IgG/PF4/heparin ternary immune complex and also to propagate formation of ?ultralarge immune complexes? (ULCs) that contain multiple IgG antibodies. Fourth, ULCs signal through Fc?RIIA receptors, activating platelets and monocytes directly and generating thrombin, which transactivates hematopoietic and endothelial cells. A non-pathogenic anti-PF4 antibody prevents tetramer formation, binding of pathogenic antibody, platelet activation and thrombosis, providing a new approach to manage HIT. An improved understanding of the pathogenesis of HIT may lead to novel diagnostics and therapeutics for this autoimmune disease. äAtomic features of an autoantigen in heparin-induced thrombocytopenia (epmc).pdf DeepDyve Pubget Overpricing