Platelet glycoprotein IV (CD36) deficiency is associated with the absence (type I) or the presence (type II) of glycoprotein IV on monocytes.
Platelet glycoprotein IV (CD36) deficiency is associated with the absence (type I) or the presence (type II) of glycoprotein IV on monocytes.
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DOI：
10.1182/blood.v83.2.392.bloodjournal832392
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发表时间：
1994-01
期刊：
影响因子：
20.3
通讯作者：
N. Yamamoto;N. Akamatsu;Hitoshi Sakuraba;H. Yamazaki;K. Tanoue
中科院分区：
文献类型：
--
作者：
N. Yamamoto;N. Akamatsu;Hitoshi Sakuraba;H. Yamazaki;K. Tanoue
血小板膜糖蛋白 (GP) IV（也称为 CD36 和 GPIIb）缺乏与 N（又名）阴性血小板有关。通过对单克隆抗 GPIV 抗体 OKM5 染色的细胞进行流式细胞术分析，我们研究了 16 名血小板缺乏 GPIV 的健康日本人的单核细胞上 GPIV 的表达。 2 名血小板 GPIV 阴性供体（I 型）的单核细胞表面不存在 GPIV，而其余 14 名血小板 GPIV 阴性供体（II 型）的单核细胞上存在 GPIV。 OKM5 染色的 II 型单核细胞的荧光强度显着 (P < .05) 低于来自血小板 GPIV 阳性供体的正常单核细胞，表明与正常单核细胞相比，II 型单核细胞上的 GPIV 表达也受到异常调节。 OKM5 在 II 型单核细胞以及正常单核细胞中诱导氧化爆发，但未能在 I 型单核细胞中诱导氧化爆发。由于 2 名患有 I 型缺陷的个体一直健康且没有表现出免疫问题，因此 GPIV 似乎对于单核细胞的正常生理功能不是必需的。在一名 I 型 GPIV 缺陷妇女的血清中检测到了抗 GPIV 抗体，该妇女从未接受过任何输血，但生下了三个表面健康的孩子。这些结果表明，I 型 GPIV 缺陷个体可能在输血或怀孕时面临产生抗 GPIV 同种抗体的风险。
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.