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Development and characterization of monoclonal antiplatelet autoantibodies
from autoimmune thrombocytopenic purpura-prone (NZW x BXSB)F1 mice
H Mizutani, RW Engelman, Y Kurata, S Ikehara and RA Good
Department of Pediatrics, University of South Florida, All Children's
Hospital, St Petersburg 33701.
Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving
autoantibodies, progressive thrombocytopenia, lupus nephritis, and
degenerative coronary vascular disease with myocardial infarction.
Platelet-associated IgG (PAIgG) on the platelet surface mediates platelet
destruction by the reticuloendothelial system in the autoimmune
thrombocytopenic purpura (ATP) of W/BF1 mice. Because the epitopes targeted
in ATP by PAIgG have not been identifiable using serum from
thrombocytopenic W/BF1 mice, we developed seven hybridomas secreting
antiplatelet monoclonal antibodies (MoAbs) using splenocytes of
thrombocytopenic W/BF1 mice. Epitopes recognized by three MoAbs were
similar to those recognized by PAIgG, because eluted IgG from platelets of
thrombocytopenic W/BF1 mice inhibited platelet binding by MoAbs in
competitive micro-enzyme-linked immunosorbent assay. Hybridoma cells or
purified Ig from the ascites of two clones (2A12 and 6A6), when injected
into nude mice produced acute thrombocytopenia, elevated the levels of
PAIgG, purpura, and megakaryocytosis. MoAbs of two clones also reacted with
single-stranded DNA or double-stranded DNA, and one of these clones (4-13)
bound to cardiolipin (CL) but was nonpathogenic in nude mice, suggesting
that anti-CL and antiplatelet autoantibodies can be distinct. On
immunoblotting analysis, antiplatelet MoAbs frequently bound a 100-Kd
platelet protein. These MoAbs contribute to an understanding of the
etiopathogenesis of ATP and the several antigens and autoantibodies
involved.
Volume 82,
Issue 3,
pp. 837-844,
08/01/1993
Copyright © 1993 by The American Society of Hematology
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