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Platelet glycoprotein IV (CD36) deficiency is associated with the absence
(type I) or the presence (type II) of glycoprotein IV on monocytes
N Yamamoto, N Akamatsu, H Sakuraba, H Yamazaki and K Tanoue
Department of Cardiovascular Research, Tokyo Metropolitan Institute of
Medical Science, Japan.
Platelet membrane glycoprotein (GP) IV (also called CD36 and GPIIb)
deficiency is associated with N(aka)-negative platelets. Using flow-
cytometric analysis of cells stained with the monoclonal anti-GPIV antibody
OKM5, we have studied the expression of GPIV on the monocytes from 16
healthy Japanese individuals whose platelets were deficient in GPIV. GPIV
was absent on the surface of monocytes from 2 platelet GPIV- negative
donors (type I), whereas it was present on the monocytes from the remaining
14 platelet GPIV-negative donors (type II). The fluorescent intensity of
OKM5-stained type II monocytes was significantly (P < .05) lower than
that of normal monocytes derived from platelet GPIV-positive donors,
suggesting that the expression of GPIV on the type II monocytes is also
abnormally regulated as compared with that on normal monocytes. OKM5
induced an oxidative burst in the type II monocytes as well as in the
normal monocytes, but it failed to induce it in the type I monocytes.
Because the 2 individuals with the type I deficiency have been healthy and
exhibited no immunologic problems, GPIV appears to be not essential for the
normal physiologic functions of monocytes. An anti-GPIV antibody was
detected in the serum from one of the type I GPIV-deficient women, who had
never received any blood transfusions but had given birth to three
apparently healthy children. These results suggest that type I
GPIV-deficient individuals may be at risk of developing an anti-GPIV
isoantibody upon blood transfusion or pregnancy.
Volume 83,
Issue 2,
pp. 392-397,
01/15/1994
Copyright © 1994 by The American Society of Hematology
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