Newborn infants have a variety of deficiencies in cell mediated host defense mechanisms. Although T-cells are known to play a major role in immune system regulation in adults, their role in the neonatal period is not well understood. Development of T-cell immune systems encompasses different maturational stages designated as memory T-cell (helper inducers) that express(CD45RO+) and naive T-cells (suppressor inducers) that express(CD45RA+). Naive T-cells can convert to memory T-cells after antigenic exposure. We hypothesized that the T-cell immune system is immature in full term newborn infants and that this immaturity contributes to their increased susceptibility to sepsis.

We compared the expression of cell surface markers on peripheral blood lymphocytes (using flow cytometry) from 15 full term newborn infants with clinical or culture positive sepsis to cord blood lymphocytes from 20 healthy full term infants and peripheral blood lymphocytes from 24 healthy adults. The majority of the T-cells from healthy and septic infants express the CD45RA+ (91 ± 2 vs 89 ± 3%, respectively); CD45RA+ was expressed on 51 ± 2% of the adult T lymphocytes (P<0.0001 vs the newborn). The expression of memory T-cells was significantly lower in healthy newborns than adults (13 ± 1 vs 60 ± 2%, P<0.0001). In septic newborn infants the expression of memory T-cells was higher than in healthy newborns (19 ± 2 vs 13 ± 1, P<0.04).

The marked predominance of naive T-cells in newborns is consistent with our hypothesis that the T-cell immune system is immature at birth. However, full term infants are capable of increasing expression of memory T-cells in response to sepsis. Further work is necessary to characterize memory T-cell function in newborn infants.