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Molecular basis of two novel and related high-prevalence antigens in the Kell blood group system, KUCI and KANT, and their serologic and spatial association with K11 and KETI
Article first published online: 8 APR 2013
© 2013 New York Blood Center. Transfusion © 2013 American Association of Blood Banks
Special Issue: Twenty Years since the Cloning of the Blood Group Genes
Volume 53, Issue 11pt2, pages 2872–2881, November 2013
How to Cite
Velliquette, R. W., Hue-Roye, K., Lomas-Francis, C., Gillen, B., Schierts, J., Gentzkow, K., Peyrard, T., von Zabern, I., Flegel, W. A., Rodberg, K., Debnath, A. K., Lee, S. and Reid, M. E. (2013), Molecular basis of two novel and related high-prevalence antigens in the Kell blood group system, KUCI and KANT, and their serologic and spatial association with K11 and KETI. Transfusion, 53: 2872–2881. doi: 10.1111/trf.12200
This study was funded in part by NIH grant R01 HL075716 (SL).
- Issue published online: 12 NOV 2013
- Article first published online: 8 APR 2013
- Manuscript Accepted: 3 MAR 2013
- Manuscript Revised: 17 FEB 2013
- Manuscript Received: 3 OCT 2012
- NIH. Grant Number: R01 HL075716 (SL)
The numerous antigens in the Kell blood group system result from missense nucleotide changes in KEL. Antibodies to antigens in this system can be clinically important. We describe six probands whose plasma contained antibodies to high-prevalence Kell antigens and discuss their relationship.
Study Design and Methods
Polymerase chain reaction amplification, direct sequencing, restriction fragment length polymorphism assays, hemagglutination, flow cytometry, and protein modeling were performed by standard methods.
Proband 1 (KUCI) and her serologically compatible sister were heterozygous for a nucleotide change in Exon 11 (KEL*1271C/T; Ala424Val). Proband 2 (KANT) was heterozygous for KEL*1283G/T (Arg428Leu) and KEL*1216C/T (Arg406Stop) in Exon 11. Red blood cells (RBCs) from Proband 1 and her sister were not agglutinated by plasma from Proband 2; however, RBCs from Proband 2 were agglutinated by plasma from Proband 1. Probands 3, 4, 5, and 6 had the KEL*1391C>T change associated with the previously reported KETI– phenotype. Proband 5 was also homozygous for KEL*905T>C encoding the K11–K17+ phenotype. Hemagglutination studies revealed an association between KUCI, KANT, KETI, and K11. Protein modeling indicated that whereas Ala424 and Arg428 are clustered, Val302 and Thr464 are not.
Ala424 in the Kell glycoprotein is associated with the high-prevalence Kell antigen, KUCI (ISBT 006032), which is detected by the antibody of Proband 1. Arg428 is associated with the high-prevalence Kell antigen, KANT (ISBT 006033). The association between KUCI, KANT, KETI, and K11 and the results of protein modeling are discussed.