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Oral tolerance, defined as hyporesponsiveness to innocuous antigens, may be explained by T-cell anergy, clonal deletion by apoptosis and active (contact-dependent) or cytokine-mediated (immune deviation) suppression exerted by subsets of regulatory T cells [55]. Important variables with regard to oral tolerance induction include genetics, age, dose and timing of postnatal oral antigen administration, antigenic structure and composition, gut epithelial barrier integrity and the degree of concurrent local immune activation (reflected by local cytokine profiles and expression of costimulatory molecules on antigen-presenting cells; fig. 1) [55].

Most children have outgrown CMA by 3 years of age, but in a minority it can become persistent. Non-IgE-mediated allergy typically resolves earlier than IgE-mediated allergy. Conversely, high specific IgE and low IgA levels to β-Lg at diagnosis and low CM-specific IgG4 during follow-up are associated with persistent CMA [56].

In an open prospective comparative study, 260 infants diagnosed with CMA (IgE-mediated CMA in 43%) were evaluated for acquisition of tolerance. The rate of children acquiring oral tolerance after 12 months of treatment was significantly higher (p < 0.05) in the groups receiving eHF-C (43.6%) or eHF-C plus LGG (78.9%) compared with the other groups: rice HF (32.6%), soy formula (23.6%) and AAF (18.2%). Binary regression analysis (coefficient B) revealed that the rate of patients acquiring tolerance at the end of the study was influenced by two factors, the IgE-mediated mechanism (B -2.05, OR 0.12, 95% CI 0.06-0.26; p < 0.001) and the formula chosen, i.e. those receiving either eHF-C (B 1.48, OR 4.41, 95% CI 1.44-13.48; p = 0.009) or, even better, eHF-C plus LGG (B 3.35, OR 28.62, 95% CI 8.72-93.93; p < 0.001) [46].

Fig. 1. Tolerance and allergy. GALT = Gut-associated lymphoid tissue.