Studies using animal models have suggested several approaches for the prevention of allergen sensitization, such as the use of mutated allergens for vaccine engineering, schedules for oral tolerance induction, Treg induction and Th1 inducer adjuvants. Furthermore, experimental protocols involving the vaccination of the mother for indirect intervention in infants should be considered because initial allergen sensitization could occur during pregnancy or early infancy [6,7]. Maternal immunization is a particularly interesting approach for the passive transference of antibodies and other factors to the fetus/newborn as a regulatory mechanism for modulating the skewed Th2 neonatal immune responses of a Th2-linked allergy profile. In addition, maternal influences on the fetus or young infant are essential for the immunological decision between tolerance and immunity in the offspring. Several approaches attempting to induce maternal IgG allergen-specific antibodies have been shown to protect rat offspring against allergic sensitization [8,9], inhibiting anti-ovalbumin IgE antibody production for up to 14 weeks after birth. The efficiency of maternal immunization is associated with the period during which immunization occurs, and immunization during early gestation is more effective at controlling the allergic response of the offspring than immunization later in gestation [10]. The complete suppression of allergen-specific IgE antibodies in the offspring depends on the presence of maternal IgG 1 antibodies. We have shown that preconception immunization on mice with the dust mite Dermatophagoides pteronyssinus or ovalbumin promoted the transference of high levels of allergen-specific IgG antibodies via transplacental/amniotic pathways In recent decades, there has been an increase in the incidence of allergic disease worldwide, particularly in children. Several environmental stimuli and host genetic factors are involved in the development of allergies and viral infections in the neonatal period. There is evidence that prenatal risk factors, such as changes in diet during pregnancy or lactation, lifestyle and cigarette smoke, can interfere with epigenetics and lead to the early development of allergies [1]. Environmental agents implicated in airway disease can induce epigenetic changes that have important implications for the development of allergic and immunologic diseases. Risk factors that contribute to the development of atopy in newborns and children require prevention strategies that are initiated in early life. There is some evidence of a positive correlation between fetus sensitization and inhalant or food allergen exposure during pregnancy, as revealed in assays of antigen-specific cellular proliferation from the umbilical cords of children from atopic mothers [2,3]. However, studies of high-risk children have shown that the priming of Th2 responses associated with persistent IgE antibody expression against dust mites occurs entirely postnatally [4]. The timing of allergen sensitization is controversial, with conflicting evidence suggesting transplacental priming versus exclusively postnatal priming. Because the absolute avoidance of environmental allergens, even in the preor post-natal stage, is not possible, ongoing and future studies aim to generate mechanistic insights that will enable the rational design of vaccines and adjuvants for pregnant or nursing mothers or neonates and, thereby, reduce the incidence of allergy symptoms in infancy and early childhood [5].