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Blood, 1 May 2001, Vol. 97, No. 9, pp. 2879-2885
TRANSFUSION MEDICINE
Molecular identification of Knops blood group polymorphisms found
in long homologous region D of complement receptor 1
Joann M. Moulds,
Peter A. Zimmerman,
Ogobara K. Doumbo,
Lalla Kassambara,
Issaka Sagara,
Dapa A. Diallo,
John P. Atkinson,
Malgorzata Krych-Goldberg,
Richard E. Hauhart,
Dennis E. Hourcade,
David T. McNamara,
Daniel J. Birmingham,
J. Alexandra Rowe,
John J. Moulds, and
Louis H. Miller
From the University of Texas-Houston Medical School,
Houston; Case Western Reserve University, Cleveland, OH; University of
Mali, Bamako, Mali; Washington University School of Medicine, St.
Louis, MO; The Ohio State University, Columbus; University of
Edinburgh, Scotland; Ortho Clinical Diagnostics, Raritan, NJ; and
National Institutes of Health, National Institute of Allergy and
Infectious Diseases, Bethesda, MD.
Complement receptor 1 (CR1) has been implicated in rosetting of
uninfected red blood cells to Plasmodium
falciparum-infected cells, and rosette formation is associated
with severe malaria. The Knops blood group (KN) is located on CR1 and
some of these antigens, ie, McCoy (McC) and Swain-Langley
(Sla), show marked frequency differences between Caucasians
and Africans. Thus, defining the molecular basis of these antigens may
provide new insight into the mechanisms of P falciparum
malaria. Monoclonal antibody epitope mapping and serologic inhibition
studies using CR1 deletion constructs localized McC and Sla
to long homologous repeat D of CR1. Direct DNA sequencing of selected
donors identified several single nucleotide polymorphisms in exon 29 coding for complement control protein modules 24 and 25. Two of these
appeared to be blood group specific: McC associated with K1590E and
Sla with R1601G. These associations were confirmed by
inhibition studies using allele-specific mutants. A sequence-specific
oligonucleotide probe hybridization assay was developed to genotype
several African populations and perform family inheritance studies.
Concordance between the 1590 mutation and McC was 94%; that between
Sla and 1601 was 88%. All but 2 samples exhibiting
discrepancies between the genotype and phenotype were found to be due
to low red cell CR1 copy numbers, low or absent expression of some
alleles, or heterozygosity combined with low normal levels of CR1.
These data further explain the variability observed in previous
serologic studies of CR1 and show that DNA and protein-based genetic
studies will be needed to clarify the role of the KN antigens in malaria.
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