Lin Jeong-Shi, Lee Li-Hsuan, Liu Hsueng-Mei, Chen Ying-Ju, Chiou Tzeon-Jye
Division of Transfusion Medicine, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Division of Hematology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Transfus Med Hemother. 2018 Jan;45(1):48-52. doi: 10.1159/000468992. Epub 2017 Sep 19.
Interleukin 6 (IL-6) is involved in regulation of immunoglobulin production. The aim of this study was to investigate the association between IL-6 single nucleotide polymorphisms (SNPs) in the IL-6 promoter and anti-E in red blood cell (RBC) transfusion recipients.
50 healthy subjects, 54 patients with RBC alloantibody anti-E (responders), and 45 patients without alloantibody (non-responders) were recruited. All patients were E antigen-negative.
All healthy subjects and patients had GG at -174 position of gene. In our healthy subjects, the frequency of the -572 CC genotype was 58%, that of the -572 CG genotype 38%, and that of the -572 GG genotype 4%. The frequency of G allele of -572 SNP in responders was significantly higher than that in non-responders, (31.5 vs. 16.7%; p = 0.020). The frequency of -572 G-positive genotypes (CG and GG) in responders was also significantly higher than that in non-responders, (55.6 vs. 31.1%; p = 0.016). The relative risk of RBC alloimmunization for patients with the -572 G-positive genotype was significantly higher than that of patients with the -572 CC genotype, (1.771 vs. 0.640; p 0.016).
C-572G gene polymorphism is significantly associated with anti-E production, with the allele G as a risk allele.
白细胞介素6(IL-6)参与免疫球蛋白产生的调节。本研究旨在探讨IL-6启动子中IL-6单核苷酸多态性(SNP)与红细胞(RBC)输血受者中抗-E的相关性。
招募了50名健康受试者、54名患有红细胞同种抗体抗-E的患者(反应者)和45名无同种抗体的患者(无反应者)。所有患者均为E抗原阴性。
所有健康受试者和患者在基因-174位置均为GG。在我们的健康受试者中,-572 CC基因型的频率为58%,-572 CG基因型的频率为38%,-572 GG基因型的频率为4%。反应者中-572 SNP的G等位基因频率显著高于无反应者(31.5%对16.7%;p = 0.020)。反应者中-572 G阳性基因型(CG和GG)的频率也显著高于无反应者(55.6%对31.1%;p = 0.016)。-572 G阳性基因型患者发生红细胞同种免疫的相对风险显著高于-572 CC基因型患者(1.771对0.640;p 0.016)。
C-572G基因多态性与抗-E产生显著相关,等位基因G为风险等位基因。