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Demonstration of platelet antigens that bind platelet‐associated autoantibodies in chronic ITP by direct immunoprecipitation procedure
Author(s) -
Tomiyama Y.,
Take H.,
Honda S.,
Furubayashi T.,
Mizutani H.,
Tsubakio T.,
Kurata Y.,
Yonezawa T.,
Tarui S.
Publication year - 1990
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1990.tb02622.x
Subject(s) - autoantibody , immunoprecipitation , platelet , antigen , antibody , immunology , medicine , splenectomy , spleen
Summary Platelet antigens that bind platelet‐associated autoantibodies in chronic idiopathic thrombocytopenic purpura (ITP) were demonstrated using a direct immunoprecipitation procedure. ITP platelets, with bound autoantibodies, were radiolabelled and solubilized, and then platelet antigen‐antibody complexes adsorbed to protein A‐bearing Staphylococcus aureus were analysed by 7.5% sodium dodecyl sulphate, polyacrylamide gel electrophoresis (SDS‐PAGE). Direct immunoprecipitation demonstrated the presence of platelet‐associated autoantibodies against glycoprotein (GP) IIb/IIIa in four of six ITP patients with an intensive band corresponding to platelet‐associated IgG. These results were confirmed by indirect immunoprecipitation using ether eluates from two ITP patients. In addition, only direct immunoprecipitation demonstrated the presence of autoantibodies against an unidentified protein having a molecular mass of 56 kDa in three of the six patients. These three ITP patients having autoantibodies against GP IIb/IIIa and against the 56 kDa protein were studied after splenectomy. Two patients, showing disappearance of autoantibodies against these antigens, attained a complete remission, and one patient, with autoantibodies against the 56 kDa protein despite splenectomy, attained only partial remission. These data suggest that autoantibodies against GP IIb/IIIa and against the 56 kDa protein may play a role in platelet destruction in some ITP patients.