There is much interest in the role of early-life events in the subsequent development of atopy and/or atopic disease. Despite the ongoing debate about the intrauterine exposure of the fetus to environmental allergens and the establishment of T-cell memory, it is clear that the immunological response of the neonate at risk of atopy is more immature than that of the neonate likely to be non-atopic. The reasons for this remain unknown, but might reflect maternally transmitted signals that adapt the neonatal immune response. An inadvertent consequence of this might be an inappropriate host response to environmental signals such as those from microbial products during early post-natal life that result in an inability to dampen neonatal T helper 2-skewed responses. The developing gastrointestinal tract and theexogenous factors that impact on this, such as microbial flora and breast milk, should therefore be a focus of investigation.