The functional immaturity of PMNs is one of the major causes of overwhelming sepsis in newborns. In this study, we observed functions and surface markers of PMNs to investigate what causes the functional immaturity of PMNs in newborns. As results, the percentage of EA rosette forming PMNs (58.5 ± 15.5%) and the chemotactic movement (0.14 ± 0.09 mm) of cord blood PMNs were significantly lower than those of adult peripheral blood PMNs (70.8 ± 9.9%, 0.60 ± 0.34 mm). Cord blood PMNs showed decreased glass adherence and ADCC activity. The expression of Fcγ RII or Fcγ RIII was a little lower than those of adult peripheral blood PMNs, but the expression of Fcγ RI (43.1 ± 26.8%) was significantly higher than that of adult peripheral blood PMNs (3.2 ± 1.8%). There was a significant difference in LFA-1 expression between EA rosette forming PMNs (92.9 ± 9.1%) and EA rosette non-forming PMNs (25.6 ± 22.6%). From these results, it is assumed that neonatal PMNs may consist of heterogeneous populations. And the relatively high percentage of EA rosette non-forming PMNs which express a low level of LFA-1 may be responsible for the functional immaturity of cord blood PMNs.