BACKGROUND: Peanut allergy has been increased in westernized countries and recently it is increasing in Korea, and the peanut allergy is one of the most potent food allergies, even though the prevalence is not high compared to other food allergies. As like other food allergies, allergen avoidance is the only therapeutic option for peanut allergy. For the mechanistic or immunologic studies of food allergy is very limited in human, so we need a good quality of animal model of food allergy. OBJECTIVE: The purpose of this study was to develop a murine model of IgE mediated peanut allergy which mimics human peanut allergy. METHOD: C3H/HeJ mice were sensitized intragastricly, at day 1, 2, 3, 7, 21 with 1 mg (Group I) or 5 mg (Group II) of crude peanut extract mixed with cholera toxin, or sensitized by intraperitoneally (1 mg, Group III) at day 1, 7, 21 with alum solution, and the Group IV mice were served as naive control. Mice were challenged intragastricly at week 5. Serum peanut specific IgE, IgG1 were measured atweekly interval, and the splenocyte proliferation assay and cytokine profiles were evaluated after challenge at week 5. RESULT: Peanut specific IgE levels markedly increased at week 3, and the IgE responses increased till week 5 in intragastricly sensitized mice (Group I and II), while the initial profound IgE responses were abrogated after week 3 in intraperitoneally sensitized mice (Group III). The IgE levels were higher in Group II compared to Group I mice, and the IgE levels were consistent with fecal peanut specific IgA levels and anaphylaxis symptom score at week 5 challenge. Peanut stimulated productions of IL-4 and INF-gamma were higher in Group I and II compared to Group III. CONCLUSION: In this experiment, we have established relatively good quality of murine model of food allergy by intragastric sensitization which showed proper peanut specific IgE responses and cytokine productions. We suggest that this model could provide a good animal model for future research in food allergy.