![]() The D VI phenotype was further confirmed by reactivity with monoclonal anti-D BS221, H41 (Biotest), and BRAD-2 (International Blood Group Reference Laboratory, Bristol, UK), as well as absence of reactivity with BS227, BS229, BS231, BS232 (Biotest) and RUM-1 (Bio Products Laboratory, Elstree, UK). As described previously, 8 blood samples in Ulm screened for differential reactivity with a monoclonal IgM anti-D (BS226 Biotest, Dreieich, Germany not reactive with D VI) and with polyclonal anti-D in antiglobulin technique were checked for the D VIphenotype by a panel of monoclonal anti-D (D-Screen Diagast, Lille, France). 17ĮDTA- or citrate-anticoagulated blood samples came from southwestern Germany (DRK-Blutspendedienst Baden-Württemberg, Ulm, Germany), northern Germany (DRK-Blutspendedienst Niedersachsen, Oldenburg) and Tyrol, Austria (Zentralinstitut für Bluttransfusion und Immunologische Abteilung Innsbruck, Innsbruck, Austria). 8, 15, 16 The majority of RhD positive individuals with allo-anti–D were D VI. D VI is reported to comprise about 6% to 10% of weak D samples 8, 15 and has a phenotype frequency of 1:6,200 in Germany (range, 0.02% to 0.05% in Caucasians). 14 D VI is the most abundant serologically defined partial D occurring among weak D samples. Severe cases of hemolytic disease of the newborn have occurred in RhD positive babies born to D VI mothers with anti-D. 12, 13 D category VI (D VI) is the clinically most important partial D. 11Today, characterization of partial D is performed by differential reactivity with monoclonal anti-D antibodies. Initially, these individuals have been classified into six distinct categories (D II to D VII, D I being obsolete) based on the mutual reactivity with polyclonal anti-D sera from immunized partial D carriers. Rare individuals carry a partial D antigen 10 and may produce alloantibodies directed against D epitopes that are lacking in their RhD protein. The D antigen comprises several different antigenic epitopes. ![]() The reconsideration of previous serologic and clinical data for partial D in view of the underlying molecular structures may be worthwhile. Genotyping strategies should take account of allelic variations in partial RhD. D VI type II and D VI type III occurred as CDe haplotypes, and D VI type I as a cDE haplotype.The distribution of the D VI types varied significantly in three German-speaking populations. The number of RhD proteins accessible on the red blood cells' surface of D VI type III was normal (about 12,000 antigens/cell D VI type I, 500 D VI type II, 2,400) based on the determination of an RhD epitope density profile. Each D VI type showed distinct immunohematologic features in flow cytometry. Thus, the D VI phenotype originated in at least three independent molecular events. We differentiated the 5′ breakpoints of D VI type I and D VI type II by a newly devised RHD-PCR. Rhesus introns 5 and 6 were sequenced and the 3′ breakpoints of all known D VI types shown to be distinct. A new genotype, hereby designated D category VI type III, was characterized as a RHD-Ce(3-6)-D hybrid allele by sequencing of the cDNA, parts of intron 1, and by PCR-restriction fragment length polymorphism (PCR-RFLP) of intron 2. Twenty-six D VI samples were detected and examined by exon-specific RHD polymerase chain reaction with sequence-specific primers (PCR-SSP). Because there was no population-based work-up, we screened three populations in central Europe for D VI. D VI red blood cells were assumed to possess very low RhD antigen density and to be caused by two RHD-CE-D hybrid alleles. Rhesus D category VI (D VI) is the clinically most important partial D.
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