An effective form of innate immunity involves naive T-cells initiating a specific response to a pathogen (1). Mononuclear phagocytes producing IL-12 upon stimulation by microbial products or direct infection are central to this response. IL-12 induces the production of IFN-γ by T-cells and NK-cells, and naive T-cells develop preferentially into T-helper-1 (Th1) lymphocytes (1).

Neonates are deficient in the production of IFN-γ, a potent macrophage-activating agent in vivo (2). Memory T cell deficiency in neonatal blood compared to adult blood (12.3 %versus 55.2 % memory cells and 87.6% vs 44.8% naive cells in cord and adult blood, respectively) has been suggested to be responsible for the neonatal deficiency of IFN-γ production (3). In a recent study, Joyner et al. proposed that decreased production of IL-12 may also be linked to IFN-γ deficiency in newborns (4). They studied group B streptococcus (GBS)-stimulated mRNA accumulation and protein secretion of both IFN-γ and IL-12 in mononuclear cells from cord and adult blood. By using reverse transcriptase polymerase chain reaction and quantitative densitometry assays, the authors compared kinetics of GBS-stimulated accumulation of IFN-γ mRNA and IL-12 mRNA (both p40 and p35 subunits) in cord and adult cells. After 12-18 h of incubation, they detected significantly decreased mRNA accumulation for both IFN- and IL-12 in cord cells compared to adults. The concentration of IFN-γ and IL-12 in suspensions of GBS-induced cord mononuclear cells was also significantly lower than in adults at 12 and 18 h. The data presented in this paper suggest that IFN-γ deficiency in neonates may be attributed, in addition to lymphocyte immaturity, to decreased production of IL-12 by cord mononuclear phagocytes.

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