Perinatal expression of the Lewis and secretor blood group systems.

Abstract

The sequential development of the expression of the Lewis and secretor gene systems in red cells and saliva was studied in normal infants by both qualitative and semiquantitative serological methods. Infants who are Lewis-positive <i>(Le/ ) </i>secretors <i>(Se/ ) </i>are red cell type Le(a –– b –– x + ) at birth; within a week they become Le(a + b –– x + ), then Le(a + b + x + ) and at approximately 2 years attain the adult phenotype Le(a –– b + x + ). In Lewis-positive <i>(Le/ ) </i>nonsecretors (<i>se/se</i>),maturation stops at the Le(a + b –– x + ) phase. Lewis-negative (<i>leile</i>) infants remain Le(a –– b –– x –– ). The salivary expression of the Lewis and secretor genes, however, are fully developed at birth. Compared to term infants, premature infants exhibit a more delayed maturation of these gene systems. These studies show the rate of maturation and tissue expressivity of the Lewis and secretor genes in the red cells and secretory tissues during the perinatal period is not synchronous; red cell expression lags behind that in saliva. The data also suggest that the <i>Le </i>gene governs the production of two antigens, Le<sup>a</sup> and Le<sup>x</sup>, and that Le<sup>x</sup> is the only antenatal red cell expression of the <i>Le </i>gene wich gives rise phenotypically to the unique Lewis type of the newborn Le(a –– b –– x + ).Le<sup>a</sup>, although repressed during intrauterine life, is activated rapidly within a few days after birth. The secretor gene activates later; its first red cell expression, the Le<sup>b</sup> antigen, may be evident between the first week and the fourth month of postnatal life. Its full expression, the complete conversion to Le(a –– b + x +) may take up to 2 years; it is during this transition phase that the second unique infantile type Le(a + b + x + ) is found. In the case of the Lewis-negative (<i>leile</i>) infant, the salivary studies suggest that the fetal <i>le </i>gene is not an amorph but is activated late in intrauterine life and undergoes a gradual but partial inactivation during the perinatal period. That the fetal <i>se </i>gene is also weakly active during the perinatal period and is then totally inactivated within the first year of life is suggested by the findings from two nonsecretor <i>(se/se) </i>infants.