Human newborns present impaired T helper type 1 cell responses, associated with a defect in the synthesis of IL‐12 by dendritic cells (DC). IL‐23 is a heterodimeric cytokine structurally related to IL‐12, implicated in protective and autoimmune responses. We recently showed that upon activation neonatal T cells up‐regulate a functional IL‐23 receptor and that this cytokine polarizes the differentiation of naive T cells. We therefore investigated the capacity of neonatal DC to secrete IL‐23. Lipopolysaccharide (LPS) stimulation induced the transcription of IL‐23(p19) mRNA in both adult and neonatal DC, in sharp contrast to the repressed IL‐12(p35) gene expression observed in neonatal cells. In comparison to adult DC, neonatal DC produced similar levels of IL‐23 protein, in reponse to Toll‐like receptor (TLR)‐2‐ and TLR‐3 ligands, and higher levels in response to TLR‐4‐ or TLR‐8 ligands. The same profile was observed in neonatal mononuclear cells. The supernatant of LPS‐stimulated DC induced the secretion of IL‐17 by polyclonally activated neonatal CD8⁺ T cells, confirming the IL‐23 bioactivity. Altogether, these observations strongly suggest that IL‐23 could play a role in the immune system of human newborns. In particular, a functional IL‐23/IL‐17 axis might compensate a suboptimal IL‐12/IFN‐γ pathway in early life.