The Kell system, a major antigenic system in human erythrocytes, possesses more than 20 different related antigens (56,57). The Kell antigens are localized on a 93-kDa red blood cell integral membrane glycoprotein (56,57). K1 and K2 are alternate, autosomally inherited, codominant alleles. The KEL gene is located on chromosome 7 (q33), spans approx 21.5 kb, contains 19 exons, and predicts a peptide of 731-amino-acid residues (58,59). At the molecular level, the difference between the K2 and K1 alleles is a single-base change within exon 6 at position 698, which results in the incorporation of methionine (ATG) for threonine (ACG) at amino acid residue 193 (58,59). K1 is an effective immunogen, being second after RhD in immunogenicity relative to other blood group antigens, and K1 antibodies can cause severe reactions to transfusion of incompatible blood, as well as hemolytic disease of the newborn. The Kell phenotype frequencies in Caucasians are 0.2%, 8.8%, and 91.0% for K1/K1, K1/K2, and K2/K2, respectively, and K1 is observed in approx 4% of the black population (60). Maternal sensitization to K1 is observed in 0.1% of all pregnancies, making anti-K1 the fourth most common antibody encountered in prenatal testing (61).
Although the administration of Rh immune globulin has led to a decrease in the number of mothers sensitized to the RhD antigen, there is no analogous treatment to prevent maternal sen-sitization to K1. However, hemolytic disease arising from maternal antibodies to other fetal antigen systems, including those of the Kell system, can be as severe as hemolytic disease resulting from anti-D antibodies. Like the RhEe system, genotyping for the KEL1 and KEL2 alleles by ASPCR is relatively straightforward, and reliable assays have been published (12,62).
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