De novo food allergy is a common phenomenon among pediatric solid organ recipients (8.5%-57%) when compared with the general
population (0.45%-10%). Other associated disorders include non–IgE-mediated immune reactions and clinical predisposition to asthma
and alterations in the oral mucosa. Originally, passive mechanisms (passive transfer of IgE and immune cells) were thought to be responsible
for acute, transient cases of food allergies with a previous history of sensitization for a specific allergen in the donor. Recently proposed
pathophysiological mechanisms to explain de novo allergies include T_H2/B-cell imbalance, regulatory T-cell (Treg) disruption, gastrointestinal
immaturity, and altered gastrointestinal permeability. Recent studies also suggest that immunosuppressive drugs, especially tacrolimus,
promote naïve T-cell differentiation into T_H2 cells, IgE-promoting cytokine production, decreased IL-5 and IL-10 levels, increased IgA
levels, and Treg disruption. Such immunological interactions, in conjunction with altered intestinal permeability, intestinal immaturity in
children, history of viral infection, and a personal history of allergies or eczema, are thought to explain most clinical cases of pediatric de
novo food allergy after solid organ transplantation reported in the literature. A better understanding of the immunological mechanisms
underpinning organ donors and recipients may unveil some of the caveats concerning therapeutic management and improve the quality
of life of affected individuals.

Key words: Allergies, Transplant, Pediatric, Calcineurin inhibitors, Treg, TH17, TH2