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Complement activation in vitro by antiplatelet antibodies in chronic immune thrombocytopenic purpura
Author(s) -
Tsubakio T.,
Tani P.,
Curd J. G.,
Mcmillan R.
Publication year - 1986
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.1365-2141.1986.tb05552.x
Subject(s) - autoantibody , platelet , antibody , immunology , thrombocytopenic purpura , complement system , in vivo , classical complement pathway , medicine , platelet lysate , in vitro , chemistry , biology , biochemistry , microbiology and biotechnology
Summary. Many chronic ITP patients have increased amounts of platelet‐associated IgG, C3, C4 and C9, suggesting in vivo complement activation. In this study, we assessed the ability of various antiplatelet antibodies (APA) to activate and deposit complement proteins and to cause platelet lysis in vitro . Platelet sensitization with rabbit APA, anti‐Pl A1 antibody (one patient), anti‐HLA antibody (two patients) and ITP autoantibodies (four patients) resulted in the deposition of C4 and C3 onto platelets in an amount proportional to the quantity of antibody‐containing sera used to sensitize the platelets. Although C9 deposition onto platelets could not be quantitatively demonstrated on platelets sensitized with ITP serum, platelet lysis ( 5 1 Cr release) was noted after incubation with each of three ITP sera and complement. When compared, ITP autoantibodies, anti‐HLA and anti‐Pl Ai antibodies activated complement to a similar degree. We conclude that some autoantibodies in chronic ITP activate the classical complement pathway. The demonstration of in vitro platelet lysis by autoantibodies and complement suggests that in vivo platelet lysis may occur in some chronic ITP patients.