PhD, Postdoctoral Researcher, Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden, and Department of Biotechnology and Biomedicine, Technical University of Denmark, Lyngby, Denmark.
PhD, Technical Director of the Nordic Reference Laboratory for Genomic Blood Group Typing, Division of Hematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University, and Department of Clinical Immunology and Transfusion Medicine, Office for Medical Services, Lund, Sweden.
Immunohematology. 2023 Apr 5;39(1):1-10. doi: 10.21307/immunohematology-2023-002. Print 2023 Apr 1.
The high-prevalence blood group antigen, Sd, had been puzzling blood bankers and transfusionists for at least a decade when it was reported in 1967. The characteristic mix of agglutinates and free red blood cells (RBCs), caused by anti-Sd, is seen with the RBCs from 90 percent of individuals of European descent. However, only 2-4 percent of individuals are truly Sd(a-) and may produce anti-Sd. The antibodies, generally considered insignificant, may cause hemolytic transfusion reactions with high-expressing Sd(a+) RBCs (e.g., the unusual Cad phenotype, which can also be polyagglutinable). The Sd glycan, GalNAcβ1-4(NeuAcα2-3)Gal-R, is produced in the gastrointestinal and urinary systems, while its origin on RBCs is more controversial. According to current theory, Sd is likely to be passively adsorbed in low amounts, except in Cad individuals, where it has been found on erythroid proteins and at higher levels. The long-standing hypothesis that encodes the Sd synthase was confirmed in 2019, since homozygosity for a variant allele with rs7224888:C produces a non-functional enzyme associated with most cases of the Sd(a-) phenotype. Thereby, the SID blood group system was acknowledged as number 038 by the International Society of Blood Transfusion. Although the genetic background of Sd(a-) was settled, questions remain. The genetic background of the Cad phenotype has not yet been determined, and the source of the RBC-carried Sd is unknown. Furthermore, the interest of Sd stretches beyond transfusion medicine. Some tantalizing examples are lowered antigen levels in malignant tissue compared with normal tissue and interference with infectious agents like , influenza virus, and malaria parasites.
高频率血型抗原 Sd 于 1967 年被报道，至少在十年前就一直困扰着血液银行家和输血学家。由抗-Sd 引起的凝集物和游离红细胞（RBC）的特征混合，在 90%的欧洲血统个体的 RBC 中可见。然而，只有 2-4%的个体真正是 Sd(a-)，可能会产生抗-Sd。这些抗体通常被认为无足轻重，但可能会与高表达 Sd(a+)RBC 发生溶血性输血反应（例如，罕见的 Cad 表型，也可能是多凝集）。Sd 聚糖 GalNAcβ1-4(NeuAcα2-3)Gal-R 在胃肠道和泌尿系统中产生，而其在 RBC 上的起源则更具争议。根据目前的理论，Sd 可能会以低量被被动吸附，除了在 Cad 个体中，在那里已经在红系蛋白上发现了更高水平的 Sd。编码 Sd 合酶的长期假说在 2019 年得到证实，因为 rs7224888:C 的变异等位基因纯合导致与大多数 Sd(a-)表型相关的非功能性酶。因此，SID 血型系统被国际输血协会确认为 038 号。尽管 Sd(a-)的遗传背景已经确定，但仍存在一些问题。Cad 表型的遗传背景尚未确定，而且 RBC 携带的 Sd 的来源也不清楚。此外，Sd 的意义超出了输血医学。一些有趣的例子是恶性组织中的抗原水平低于正常组织，以及与感染因子如 、流感病毒和疟原虫的干扰。
