Food allergy is a phenomenon in which adverse immune reactions are caused after intake of foods. Oral tolerance is the state of unresponsiveness of the immune system to foods administered via an oral route. The mechanism for the failure of acquiring oral tolerance in food allergy patients remains unclear. Recently, the hypothesis, that allergic sensitization results from cutaneous exposure and that tolerance occurs as results of oral exposure to food, has been proposed. In this study, we investigated the balance of the relationship between oral tolerance and sensitization via skin to use murine food allergy models. We have already reported the food allergy model using ovalbumin (OVA) in which BALB/c mice were sensitized by intraperitoneal injection of OVA (IP-model). Oral tolerance was induced by oral administration of OVA before the sensitization. The induced oral tolerance in IP-model prevented increasing OVA-specific IgE and inhibited decreasing body temperature and diarrhea as symptoms of food allergy. In another food allergy model, the mice were conducted epicutaneous sensitization for OVA(EC-model). Oral tolerance in EC-model was broken and OVA-specific IgE increased slightly. These results might indicate that percutaneous load of allergen could break oral tolerance for food.