Expression of the Complement Receptors CR1 and CR3 and the Type III Fcγ Receptor on Neutrophils from Newborn Infants and from Fetuses with Rh Disease

ABSTRACT: Developmental defects in neutrophil function, including diminished expression of plasma membrane receptors, may play an important role in the susceptibility of the newborn infant

to infection. We used monoclonal antibodies and flow cytometry to study the expression of complement receptor type one (CR1), complement receptor type three (CR3), and Fcγ receptor type

three (FcRIII) on neutrophils from six fetuses with Rh disease, 10 preterm infants, nine term infants, and nine adults. Expression of the complement receptors on unstimulated cells was

similar for all groups, but significant diffences in complement receptor expression were observed after stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP). Fetal, preterm, and

term infant neutrophils expressed less CR3 than FMLP-stimulated neutrophils of adults [61 ± 2, 48 ± 4, and 66 ± 4% (mean ± SEM) of the mean for adults, p < 0.05]. FMLP-stimulated CR1

expression for these groups was 61 ± 6, 73 ± 6, and 91 ± 9% of the adult mean (p < 0.05, fetal versus term infant and adult). Expression of both CR3 and CR1 increased with postconceptional

age in the infants (r2 = 0.49, p < 0.001 for CR3; r2 = 0.23, p < 0.05 for CR1). Neutrophils of the preterm and term infants expressed less FcRIII than adult neutrophils (68 ± 10 and 77 ± 7%

of the adult mean, p < 0.05, for FMLP-stimulated cells), whereas fetal neutrophil FcRIII expression did not differ from that of the adult. The fluorescence distributions showed a peak for

eosinophils that was distinct from the FMLP-stimulated neutrophil peak, allowing separate analysis for the two cell types. Eosinophils constituted an unexpectedly large proportion of

granulocytes in fetuses with Rh disease, averaging 61% of granulocytes in seven specimens at 20 to 26 wks gestation and 37% in 11 specimens at 28 to 34 wks.

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