ABSTRACTDevelopmental 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 Fc&ggr;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 withN‐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, fetalversusterm 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 FcRIIIthan adult neutrophils (68 ± 10 and 77 ± 7% of the adult mean,p< 0.05, for FMLP‐stimulated cells), whereas fetal neutrophil FcRIIIexpression 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. (Pediatr Res28: 120‐126, 1990)AbbreviationsCR1, complement receptor type one (CD35)CR3, complement receptor type three (CD11b/CD18)FcRIII, Fc&ggr;receptor type three (CD16)FMLP,N‐formyl‐methionyl‐leucyl‐phenylalanine