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A platelet membrane glycoprotein (GP) deficiency in healthy blood donors:
Naka- platelets lack detectable GPIV (CD36)
N Yamamoto, H Ikeda, NN Tandon, J Herman, Y Tomiyama, T Mitani, S Sekiguchi, R Lipsky, U Kralisz and GA Jamieson
American Red Cross Cell Biology Laboratory, Rockville, MD 20855.
It has recently been shown that the Naka antigen, which is absent in 3% to
11% of Japanese blood donors, is expressed on platelet glycoprotein IV
(GPIV; CD36) (Tomiyama et al, BLOOD, 75:684, 1990). In the present studies,
flow cytometry was used to distinguish differences in the reactivity of
Naka+ and Naka- platelets with both OKM5, a monoclonal antibody that
recognizes an epitope on GPIV, and with polyclonal anti- GPIV antibody.
OKM5 was also used to screen 871 platelet concentrates prepared from
healthy US blood donors. Three of these showed markedly deficient binding
of 125I-OKM5 or an incidence of 0.34%. Two of these donors were re-accessed
and showed less than 1% binding of 125I-OKM5 as compared with 10,300 +/-
1,500 binding sites per platelet in controls (n = 4). Platelets from these
two US donors were radiolabeled (125I, 3H) and compared with control
platelets and with platelets from Japanese Naka+ and Naka- donors by
crossed immunoelectrophoresis, protein blots, immunoprecipitation, and
two-dimensional gel electrophoresis. GPIV could not be detected by any of
these techniques in the Naka- platelets nor in the donors whose platelets
showed deficient binding of OKM5. These results suggest that GPIV functions
as an isoantigen rather than an alloantigen in immunizing Naka- platelet
recipients. This is the first report of the absence of a major platelet
membrane GP in healthy blood donors.
Volume 76,
Issue 9,
pp. 1698-1703,
11/01/1990
Copyright © 1990 by The American Society of Hematology
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