Adsorption of cold agglutinins with rabbit red blood cells.

CONCLUSIONS: Cold-reactive autoagglutinins may mask the presence of underlying clinically significant alloantibodies. Adsorption with rabbit red blood cells (RBCs) or stroma can remove cold autoagglutinins found in the patient's plasma/serum that are directed towards antigens expressed on the surface of rabbit RBCs. By removing these cold autoagglutinins, it is then possible to determine whether any underlying alloantibody reactivity is present. Although this method may also unintentionally adsorb alloantibodies directed towards antigens found on rabbit RBCs, it is still a widely used and convenient method to remove cold autoagglutinins.

The JR blood group system: identification of alleles that alter expression.

BACKGROUND: The ABCG2 gene encodes antigens of the JR blood group system. Red blood cells (RBCs) from individuals homozygous for ABCG2 null alleles are nonreactive with polyclonal and monoclonal anti-Jr(a) . However, some RBCs have been defined as Jr(a+(W) /-) or Jr(a-), particularly when tested with polyclonal anti-Jr(a) . In an effort to resolve these apparent serologic ambiguities, the current study was undertaken. STUDY DESIGN AND METHODS: Hemagglutination of RBCs from two individuals known to express a single copy of functional ABCG2 were compared to RBCs from eight unrelated, previously characterized, Jr(a+(W) /-) donors. Standard polymerase chain reaction-based methods were used to characterize ABCG2 alleles. RESULTS: Two monoclonal anti-Jr(a) clones agglutinated RBCs from the eight Jr(a+(W) /-) study subjects. Two of these subjects were homozygous for a missense ABCG2 change (c.1858A; Asp620Asn). Two were heterozygous for two missense changes; one was c.1858G>A and c.421C>A (Asp620Asn; Gln141Lys), and the other was c.1714A>C and c.421C>A (Ser572Arg; Gln141Lys). The remaining four subjects were heterozygous for c.421C>A (Gln141Lys), and for one of four null alleles. CONCLUSIONS: We have identified three ABCG2 alleles that are newly associated with weakened Jr(a) expression. One of these is novel, the missense allele c.1714A>C (Ser572Arg) and two that have been previously described c.421C>A (rs2231142; Gln141Lys) and c.1858G>A (rs34783571; Asp620Asn). In addition, we found a novel, presumed null allele, c.1017_1019delCTC (Ser340del).