A platelet membrane glycoprotein (GP) deficiency in healthy blood donors: Naka- platelets lack detectable GPIV (CD36).
A platelet membrane glycoprotein (GP) deficiency in healthy blood donors: Naka- platelets lack detectable GPIV (CD36).
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DOI：
10.1182/blood.v76.9.1698.1698
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发表时间：
1990
期刊：
影响因子：
20.3
通讯作者：
N. Yamamoto;H. Ikeda;N. Tandon;J. Herman;Y. Tomiyama;T. Mitani;S. Sekiguchi;Robert Lipsky;U. Kralisz;G. Jamieson
中科院分区：
文献类型：
--
作者：
N. Yamamoto;H. Ikeda;N. Tandon;J. Herman;Y. Tomiyama;T. Mitani;S. Sekiguchi;Robert Lipsky;U. Kralisz;G. Jamieson
最近已经表明，纳卡抗原（其在3%至11%的日本献血者中不存在）在血小板糖蛋白IV（GPIV; CD 36）上表达（Tomiyama等，BLOOD，75：684，1990）。在本研究中，流式细胞术用于区分纳卡+和纳卡-血小板与OKM 5（一种识别GPIV上的表位的单克隆抗体）和多克隆抗GPIV抗体的反应性差异。OKM 5还用于筛选从健康美国献血者制备的871份血小板浓缩物。其中3例显示125 I-OKM 5结合明显缺陷，发生率为0.34%。这些供体中的两个被重新访问，并且显示出小于1%的125 I-OKM 5结合，而对照中每个血小板有10，300 +/-1，500个结合位点（n = 4）。对这两名美国供体的血小板进行放射性标记（125 I，3 H），并通过交叉免疫电泳、蛋白质印迹、免疫沉淀和二维凝胶电泳与对照血小板以及日本纳卡+和纳卡-供体的血小板进行比较。在纳卡-血小板和血小板显示OKM 5结合缺陷的供体中，GPIV不能通过任何这些技术检测到。这些结果表明，GPIV功能作为一个同种抗原，而不是同种异体抗原免疫纳卡-血小板受体。这是第一次报告的情况下，一个主要的血小板膜糖蛋白在健康献血者。
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.