Defective interferon gamma production in neonatal T cells is independent of interleukin-2 receptor binding.

Newborns are more susceptible to fungal, viral, protozoan, and certain bacterial infections than adults. This susceptibility is due in part to a decreased interferon gamma (IF gamma) production. The present investigation focuses on the role of the IL-2 receptor in the deficient IF gamma production in neonatal T cells. IL-2-induced IF gamma production in unstimulated neonatal cord blood and adult peripheral T cells was comparable, but the IF gamma production in CD3-stimulated neonatal T cells was only 20% of the adult production. Neonatal and adult T cells showed no difference in the expression of the 55-kD alpha and 75-kD beta chains of the IL-2 receptor. Blocking of the 55-kD alpha chain of the IL2 receptor with TAC MAb resulted in a marginal reduction in IF gamma release from unstimulated or CD3-stimulated neonatal T cells cultured in the presence of IL-2. In contrast, blocking of the 55-kD alpha chain of the IL-2 receptor in adult T cells caused a 92% and 73% inhibition in IF gamma production in unstimulated and stimulated T cells, respectively. Blocking of the 75-kD beta chain of the IL-2 receptor with TU27 MAb had a marginal effect in both unstimulated and CD3-stimulated neonatal and adult lymphocytes. Binding studies with unstimulated cord blood T cells using [125I]-IL-2 showed a binding affinity that corresponded with the intermediate affinity IL-2 receptor. In CD3-stimulated cord blood T cells, a high-affinity receptor was found.(ABSTRACT TRUNCATED AT 250 WORDS)