Anti‐U‐like as an alloantibody in S−s−U− and S−s−U+ var black people

BACKGROUND: 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.