The rising incidence of food allergy in children underscores the importance of environmental exposures; however, genetic factors play a major role. How the environment and genetics interact to cause food allergy remains unclear. The landmark Learning Early About Peanut Allergy (LEAP) clinical trial established that early peanut introduction protects high-risk infants, consistent with the tolerizing effects of gut exposure. In this issue of the JCI, Kanchan et al. leveraged the LEAP trial data to examine molecular genetic mechanisms of early sensitization. A previously identified HLA risk allele for peanut allergy (DQA1*01:02) was associated with peanut-specific IgG4 levels in consumers. Notably, IgG4 antibodies likely provide protection by reducing the binding of allergen to IgE. The association of the same allele with peanut allergy in avoiders while potentially conferring protection in consumers reinforces the need to integrate genetic information toward a personalized therapeutic strategy for the best outcome in addressing food allergies.

中文翻译：

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早期花生引入在环境与遗传学相互作用中胜过 HLA-DQA1*01:02 等位基因

儿童食物过敏发病率的上升凸显了环境暴露的重要性；然而，遗传因素起着重要作用。环境和遗传如何相互作用导致食物过敏仍不清楚。具有里程碑意义的早期花生过敏 (LEAP) 临床试验表明，早期引入花生可以保护高危婴儿，这与肠道暴露的耐受作用一致。在本期JCI, Kanchan 等人。利用 LEAP 试验数据来检查早期致敏的分子遗传机制。先前确定的花生过敏 HLA 风险等位基因 (DQA1*01:02) 与消费者中花生特异性 IgG4 水平相关。值得注意的是，IgG4 抗体可能通过减少过敏原与 IgE 的结合来提供保护。相同等位基因与回避者的花生过敏相关，同时可能为消费者提供保护，这加强了将遗传信息整合到个性化治疗策略中的需求，以获得解决食物过敏的最佳结果。