Complement receptor 1 red cell expression is not controlled by the In(Lu) gene.

Abstract

The In(Lu) gene reportedly suppresses several blood group antigens that are not part of the Lutheran system, including the high-incidence antigens of the Knops blood group system. Because complement receptor 1 (CR1), which is known to carry the Knops system antigens, has a red cell (RBC) expression polymorphism, the role of In(Lu) in the expression of the Knops system antigens was reinvestigated. Blood samples from nine donors having the Lu(a-b-) phenotype were obtained and immediately phenotyped for Lu(b), Kn(a), McC(a), Sl(a), and Yk(a). The samples were also tested for Lu(a), P1, and AnWj. Immunoblots were performed to study both the CR1 and Lutheran glycoproteins from these donors. RBC expression of CR1 was quantified with an enzyme-linked immunosorbent assay, and the genetic inheritance of the high-expression (H) or low-expression (L) allele for CR1 was determined by Southern blot. Lu(b) was demonstrable only by absorption and elution techniques on all nine samples; however, the high-incidence Knops system antigens were readily detectable by hemagglutination. Two Lu(a-b-) donors (sibs) demonstrated weak Lutheran glycoprotein bands of 78 and 85 kDa on immunoblots, while the other seven Lu(a-b-) samples had no detectable glycoprotein. All donors had CR1*1, and one donor also had CR1*2 on immunoblot. Only one donor was homozygous for the L allele, and all had RBC copy numbers of CR1 within the normal range. Nine donors with the Lu(a-b-) phenotype showed suppression of the Lutheran system antigens but normal expression of CR1 glycoprotein and the Knops system blood group antigens. This suggests that the genes that suppress Lutheran system antigens do not suppress CR1 or its related blood group antigens.