A platelet membrane glycoprotein (GP) deficiency in healthy blood donors: Naka- platelets lack detectable GPIV (CD36)

Abstract

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.

CD36 deficiency protects against malarial anaemia in children by reducing Plasmodium falciparum‐infected red blood cell adherence to vascular endothelium

“…1997), results from this study show CD36 to be the major ligand for cytoadherence of field isolates of P. falciparum. In line with previous findings elsewhere (Yamamoto et al. 1990; Greenwalt et al.…”

Human platelet antigens in Burmese, Karen and north‐eastern Thais

“…In addition, recent studies indicated that immunisation against CD36 represents another cause of alloimmune‐mediated thrombocytopenia amongst Asian populations (Hayashi & Hirayama, ). The incidence of CD 36 deficiency in Asians is approximately 2–5% (Yamamoto et al , ; Urwijitaroon et al , ; Li et al , ).…”

Two cases of platelet transfusion refractoriness associated with anti‐CD36

“…Individuals with Type I deficiency lack CD36 on PLTs and monocytes, while individuals with Type II deficiency lack CD36 only on PLTs 17 . No clinical symptoms appear to be associated with either type of CD36 deficiency 4,5,12 . It is thought that primarily individuals with Type I deficiency are at risk of immunization against the protein.…”

“…Antibodies against a novel PLT antigen, termed anti‐Nak a , were first described in a Japanese acute myelogenous leukemia (AML) patient refractory to PLT transfusions 2 . It was later shown that the Nak a antigen was located on PLT glycoprotein (GP) IV, or CD36, and individuals with anti‐Nak a lacked CD36 on their PLTs and therefore had become isoimmunized, rather than alloimmunized 3‐5 . CD36 deficiency varies widely between ethnic groups, with a frequency of 3% to 11% in Asians, 8% in sub‐Saharan Africans, and less than 0.4% in Caucasians 6‐8 .…”