Abstract
Food allergy (FA) is an exacerbated immune system response to harmless food antigens following sensitization. The incidence of FA has risen significantly over the past two decades, a trend often attributed to modern lifestyle factors such as dietary patterns, antibiotic use, and urban environments. Sensitization may result from a compromised intestinal barrier caused by inflammatory bowel diseases, genetic predisposition, or a combination of both. These conditions trigger an inflammatory response involving mechanisms such as the activation of Toll-Like Receptors (TLRs), which recognize pathogen-associated molecular patterns. This review examines the intestine's role as a key antigen-sensing organ through three critical components: a) gut-associated lymphoid tissue, b) the mucosal immune system, and, c) the intestinal microbiota in the development of FA. The role of TLRs (particularly TLR2 and TLR4) in recognizing bacterial membrane-derived compounds (e.g., lipopolysaccharides) and how commensal bacteria generate TLR ligands that influence allergen sensitization vs. tolerance is discussed. The importance of candidate gene polymorphisms encoding TLR proteins and other molecules associated with tolerance and sensitization to food antigens is also commented on. Finally, future research directions and preventive strategies to mitigate FA risk and development are suggested.