The steep rise in food allergy (FA) has evoked environmental factors involved in disease pathogenesis, including the gut microbiota, diet, and their metabolites. Early introduction of solid foods synchronizes with the “weaning reaction,” a time during which the microbiota imprints durable oral tolerance. Recent work has shown that children with FA manifest an early onset dysbiosis with the loss of Clostridiales species, which promotes the differentiation of ROR-γt⁺ regulatory T cells to suppress FA. This process can be reversed in pre-clinical mouse models by targeted bacteriotherapy. Here, we review the dominant tolerance mechanisms enforced by the microbiota to suppress FA and discuss therapeutic intervention strategies that act to recapitulate the early life window of opportunity in stemming the FA epidemic.

食物过敏（FA）的急剧上升引发了疾病发病机制中涉及的环境因素，包括肠道微生物群、饮食及其代谢物。早期引入固体食物与“断奶反应”同步，在此期间微生物群留下持久的口服耐受性。最近的研究表明，患有 FA 的儿童表现出早期发病的生态失调，伴有梭状芽胞杆菌物种的丧失，这会促进 ROR-γt ⁺调节性 T 细胞的分化以抑制 FA。在临床前小鼠模型中，可以通过靶向细菌疗法逆转这一过程。在这里，我们回顾了微生物群强制执行的抑制 FA 的主要耐受机制，并讨论了可重现生命早期机会窗口以阻止 FA 流行的治疗干预策略。