Wagner Thomas, Körmöczi Günther F, Buchta Christoph, Vadon Maria, Lanzer Gerhard, Mayr Wolfgang R, Legler Tobias J
Department of Blood Group Serology and Transfusion Medicine, Medical University of Graz, Graz, Austria.
Transfusion. 2005 Apr;45(4):520-6. doi: 10.1111/j.0041-1132.2005.04256.x.
No data are available on the immunogenicity of extremely weak D variants called DEL. Evaluation of alloanti-D formation in a D- female patient after transfusion of apparently D- blood from an Austrian donor led to discovery of a so far unknown DEL type.
Standard blood group serologic methods were applied. Molecular typing, RHD sequencing, and D epitope mapping was performed and the absolute D antigen density determined.
After transfusion of RBCs typed D- by routine serology, the recipient developed alloanti-D. Further evaluation with an indirect antiglobulin test confirmed donor RBCs to be D-. Molecular typing, however, demonstrated the presence of the RHD gene in one donor, and RHD sequencing revealed a deletion of four nucleotides in RHD intron 5 (RHD IVS5-38del4) as the only difference compared to the normal RHD gene. Adsorption-elution techniques demonstrated a DEL phenotype without apparent loss of D epitopes.
This study documents the clinical significance of the DEL phenotype in blood units that was capable of inducing anti-D in a recipient. Qualitative data are provided on D epitope expression in DEL RBCs.
关于极弱的D变异体DEL的免疫原性尚无数据。对一名D阴性女性患者输注来自奥地利供血者的看似D阴性血液后同种抗-D形成情况的评估,导致发现了一种迄今未知的DEL类型。
应用标准血型血清学方法。进行分子分型、RHD基因测序和D抗原表位定位,并测定绝对D抗原密度。
接受常规血清学检测为D阴性的红细胞输注后,受血者产生了同种抗-D。通过间接抗球蛋白试验进一步评估证实供血者红细胞为D阴性。然而,分子分型显示一名供血者存在RHD基因,RHD基因测序显示与正常RHD基因相比,唯一的差异是RHD内含子5中有四个核苷酸缺失(RHD IVS5-38del4)。吸附-洗脱技术显示为DEL表型,且D抗原表位无明显丢失。
本研究证明了DEL表型在血液制品中的临床意义,该表型能够在受血者体内诱导产生抗-D。提供了关于DEL红细胞中D抗原表位表达的定性数据。