S, s, and U antigens belong to the MNS system. They are carried by glycophorin B (GPB), encoded by GYPB. Black people with the low-prevalence S−s− phenotype, either U− or U+var, can make a clinically significant anti-U. Anti-U-like, a cold immunoglobulin G autoantibody quite commonly observed in S−s+U+ black persons, was previously described to be nonreactive with ficin-, α-chymotrypsin-, and pronase-treated red blood cells (RBCs); nonreactive or weakly reactive with papain-treated RBCs; and reactive with trypsin-treated RBCs. Here we describe, in S−s− people from different molecular backgrounds, an alloantibody to a high-prevalence GPB antigen, which presents the same pattern of reactivity with proteases as autoanti-U-like.STUDY DESIGN AND METHODS:
Four S−s− patients with an alloantibody to a high-prevalence GPB antigen were investigated by serologic and molecular methods.RESULTS:
An alloantibody was observed in two S−s−U−/Del GYPB, one S−s−U+var/GYPB(P2), and one S−s−U+var/GYPB(NY) patients. As this alloantibody showed the same pattern of reactivity with proteases as autoanti-U-like, we decided to name it “anti-U-like.” Anti-U-like made by the two S−s−U− patients was reactive with the S−s−U+var RBCs of the two other patients.CONCLUSION:
S−s−U−/Del GYPB, S−s−U+var/GYPB(P2), and S−s−U+var/GYPB(NY) patients can make an alloanti-U-like. Anti-U-like made by S−s−U− people appears reactive with GYPB(P2) and GYPB(NY) RBCs, which both express a weak and partial U-like reactivity. We recommend transfusing S−s−U− RBCs in S−s−U− patients showing alloanti-U-like. Our study contributes to a better understanding of alloimmunization to GPB in black people and confirms importance of genotyping in S−s− patients, especially those with sickle cell disease to be frequently transfused.