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Different specificities of platelet-associated and plasma autoantibodies to
platelet GPIIb-IIIa in patients with chronic immune thrombocytopenic
purpura
K Fujisawa, P Tani, TE O'Toole, MH Ginsberg and R McMillan
Department of Molecular and Experimental Medicine, Scripps Clinic and
Research Foundation, La Jolla, CA 92037.
Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disorder due
to antiplatelet autoantibodies, many of which are directed against platelet
membrane glycoprotein (GP) IIb-IIIa or GPIb-IX. In a recent study, we
described plasma autoantibodies from 13 selected ITP patients, which
required the presence of the putative GPIIIa cytoplasmic region for
antibody binding. Since this region may not be available for antibody
binding under physiologic conditions, we evaluated the frequency of binding
to this or other regions of GPIIb- IIIa by platelet-associated and plasma
autoantibody from a group of chronic ITP patients. We studied
platelet-associated autoantibodies in 27 patients and plasma antibodies in
21 patients; in 15 patients, both were studied. To determine if
autoantibodies were directed to the cytoplasmic portion of GPIIIa or to
another portion of the GPIIb-IIIa molecule, antibody eluted from patient
platelets or plasma antibody was tested in an antigen capture assay for
binding to GPIIb-IIIa obtained from Chinese hamster ovary (CHO) cells
transfected with GPIIb and either intact GPIIIa or GPIIIa lacking the
carboxy terminal 35 residues. Of the 21 plasma autoantibodies tested, 13
bound primarily to the carboxy terminus of GPIIIa and eight to other
epitopes. Conversely, all 26 platelet-associated autoantibodies, including
eight of the 13 with anti-carboxy terminus antibodies, bound to epitopes in
other regions of GPIIb-IIIa. Comparison of the degree of antibody
adsorption by intact or lysed platelets indicated that epitopes on the
c-terminal region of GPIIIa are relatively inaccessible on the surface of
intact washed platelets when compared with other epitopes. We conclude that
the importance of plasma autoantibodies in chronic ITP patients should be
interpreted cautiously, since their specificity may differ from that of
antibodies bound to the platelet. Whether antibodies against the c-
terminus of GPIIIa are of pathogenetic importance remains to be determined,
although patients with these antibodies have particularly severe disease.
Volume 79,
Issue 6,
pp. 1441-1446,
03/15/1992
Copyright © 1992 by The American Society of Hematology
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