Abstract Allergic disorders, manifest by T helper 2 (Th2) type immune responses to environmental antigens, are rapidly increasing in children. Regulatory T cells (Tregs) limit Th2 responses, and Treg deficiencies are seen in children with allergic disorders, implying that Treg deficiencies or dysfunction underlie the pathogenesis of Th2 mediated disease. What incurs Treg deficiency and its relationship to the increasing incidence of allergy is unknown, however, studies have shown that the intestinal microbiota plays an important role in regulating Treg differentiation during early life. With this in mind we explored whether oral exposure to specific antibiotics in early life altered Treg populations and predisposed to Th2 responses. We found that exposure of mice to a combination of broad spectrum oral antibiotics between days 10 and 20 of life abrogated tolerance to a dietary antigen, ovalbumin (Ova). Exposure of mice to single antibiotics of varying spectra between days 10 and 20 of life had a range of effects from abrogation of oral tolerance to the spontaneous development of Th2 responses manifested by increased levels of IL-13 in the serum in the absence of challenge. Ongoing studies are evaluating the effect of the respective antibiotic regimens on the intestinal microbial community using 16S bacterial DNA sequencing, with the aim to link alterations in the microbial composition to the immunological profile of the respective treatment groups. In summary, our results show that disruption of the intestinal microbiota by exposure to specific antibiotics during a period in early life results in loss of Tregs, promotes Th2 immunity, and impair establishment of oral tolerance to dietary antigen.