Biomedical Sciences Program, Graduate School, Khon Kaen University, Khon Kaen, Thailand.
Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.
Transfusion. 2020 Apr;60(4):847-854. doi: 10.1111/trf.15737. Epub 2020 Mar 4.
Anti-CD36s, developing after transfusion or during pregnancy, play an important role in immune-mediated bleeding disorders among Asian populations. Currently, little is known about the clinical relevance of anti-CD36. Here, we aimed to determine the frequency of CD36 deficiency in Thais by analyzing CD36 expression on cell surfaces and in plasma.
The expression and deficiency of CD36 on platelets and monocytes were determined by flow cytometry. Mutations in the CD36 gene were analyzed by nucleotide sequencing. Soluble CD36 (sCD36) in plasma was quantified with enzyme-linked immunosorbent assay.
Fifteen of 700 blood donors (2.14%) were identified as CD36 deficient. The frequencies of Type I and II CD36 deficiency were 0.43% and 1.71%, respectively. Type I individuals exhibited c.1163A > T, c.429 + 4insG, and c.1156C > T. Type II individuals exhibited c.879 T > C, c.329-330delAC, c.818 + 108delAACT, c.1125 + 13C > A, and c.1163A > T. CD36 on donor platelets (n = 685) showed a wide distribution of expression levels (mean fluorescence intensity, 16.71 ± 8.68). In the normal phenotype (n = 14), sCD36 concentration was 58.84 ± 11.68 ng/mL, which was significantly correlated with platelet CD36 expression (r = 0.8551). In Type II-deficient individuals (n = 6), a similar sCD36 concentration was detected (53.67 ± 8.17 ng/mL). However, sCD36 could not be detected in Type I individuals (n = 3).
CD36 Type I deficiency was found, indicating the potential for immune-mediated platelet disorders in Thais. However, the underlying mutations differed from those reported in Japan and China. Interestingly, sCD36 could not be detected in plasma of Type I-deficient individuals. This finding may lead to the use of plasma to identify individuals at risk and to allow screening of large cohorts.
抗 CD36 在输血后或怀孕期间产生，在亚洲人群的免疫介导性出血性疾病中发挥重要作用。目前，人们对 CD36 的临床意义知之甚少。在这里，我们通过分析细胞表面和血浆中的 CD36 表达来确定泰国人 CD36 缺乏的频率。
通过流式细胞术测定血小板和单核细胞上 CD36 的表达和缺乏。通过核苷酸测序分析 CD36 基因的突变。用酶联免疫吸附试验定量测定血浆中的可溶性 CD36(sCD36)。
在 700 名献血者中发现 15 名（2.14%）为 CD36 缺乏。I 型和 II 型 CD36 缺乏的频率分别为 0.43%和 1.71%。I 型个体表现为 c.1163A> T、c.429+4insG 和 c.1156C>T。II 型个体表现为 c.879T>C、c.329-330delAC、c.818+108delAACT、c.1125+13C>T 和 c.1163A>T。供者血小板上的 CD36（n=685）表现出表达水平的广泛分布（平均荧光强度，16.71±8.68）。在正常表型（n=14）中，sCD36 浓度为 58.84±11.68ng/mL，与血小板 CD36 表达呈显著相关（r=0.8551）。在 II 型缺乏个体（n=6）中，检测到类似的 sCD36 浓度（53.67±8.17ng/mL）。然而，在 I 型个体（n=3）中未检测到 sCD36。
发现 CD36 I 型缺乏，表明泰国人存在免疫介导性血小板疾病的潜在风险。然而，潜在的突变与日本和中国报道的不同。有趣的是，在 I 型缺乏个体的血浆中无法检测到 sCD36。这一发现可能导致使用血浆来识别有风险的个体，并允许对大样本进行筛查。
