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D variants at the RhD vestibule in the weak D type 4 and Eurasian D clusters
University Hospital, Ulm.
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2009 (English)In: Transfusion, ISSN 0041-1132, E-ISSN 1537-2995, Vol. 49, no 6, 1059-1069 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: One branch of the RHD phylogenetic tree is represented by the weak D type 4 cluster of alleles with F223V as the primordial amino acid substitution. F223V as well as a large number of further substitutions causing D variants are located at the extracellular RhD protein vestibule, which represents the entrance to the transmembraneous channel of the RhD protein.

STUDY DESIGN AND METHODS: RHD and RHCE nucleotide sequences were determined from genomic DNA and cDNA. D epitope patterns were established with commercial monoclonal anti-D panels.

RESULTS: The RHD alleles DOL-1 and DOL-2 had the two amino acid substitutions M170T (509T>C) and F223V (667T>G) in common. DOL-2 harbored the additional substitution L378V (1132C>G). Both alleles were observed in Africans and are probably evolutionary related. DMI carried M170I (510G>A), which differed from the DOL-typical substitution. DFW and DFL harbored the substitutions H166P (497A>C) and Y165C (494A>G). The antigen densities of DOL-1, DFL, and DFW were only moderately reduced.

CONCLUSION: DOL-1 and DOL-2 belong to the weak D type 4 cluster of RHD alleles. Together with DMI, DFL, and DFW they represent D variants with amino acid substitutions located at extracellular loops 3 or 4 lining the RhD protein vestibule. These substitutions were of minor influence on antigen density while adjacent substitutions in the transmembraneous section caused weak D antigen expression. All these D variants were partial D and alloanti-D immunizations have been observed in DOL-1, DMI, and DFL carriers. The substitution at position 170 causes partial D although located deep in the vestibule.

Place, publisher, year, edition, pages
2009. Vol. 49, no 6, 1059-1069 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-53044DOI: 10.1111/j.1537-2995.2009.02102.xOAI: diva2:286554
Available from: 2010-02-02 Created: 2010-01-14 Last updated: 2010-03-31Bibliographically approved

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Transfusion MedicineFaculty of Health SciencesDepartment of Clinical Immunology and Transfusion Medicine
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