Alloantibody‐Induced Impaired Neonatal Expression of a Red Blood Cell Antigen Associated with Maternal Alloimmunization

Abstract

Animals genetically capable of making certain gene products have been shown to have the production of such products completely or partially suppressed by exposure in utero or neonatally to antibodies specific for that gene product. This alloantibody-induced depression of expression of a specific antigenic determinant has yet to be shown to occur in man. The McCoya red blood cell antigen is reported to be well developed at birth. However, 2 children born to mothers with high-titer McCoya antibodies in their serum, phenotyped as McCoy (a-) at birth and, on retesting their red blood cells, 1 at 5 months and the 2nd at 11 months, both phenotyped as McCoy (a+). It is possible that this lack of expression of the McCoya antigen at birth represents a characteristic of an obligate heterozygote. However, on testing 50 random umbilical cord red blood cell samples with two potent McCoya antisera, only 1 was found to be negative. If the negative phenotype were a characteristic of an obligate heterozygote at birth, then the neonatal incidence of the McCoy (a-) phenotype should have been significantly (p less than 10(-4)) high in our random cord blood sample than observed (expected 11). The impaired expression of the McCoya antigen on the red blood cells of these 2 infants at birth, in conjunction with evidence of maternal alloimmunization, strongly suggests alloantibody-induced antigenic suppression of the McCoya antigen as a probable cause.