Moneret-Vautrin Denise-Anne
L'Académie nationale de médecine.
Bull Acad Natl Med. 2012 Jun;196(6):1131-40.
Food allergy originates from physiological fetal Th2 polarization. The normal shift towards Th1 dominance during the first months of life is defective in the atopic infant. Several factors are critical for the development of food allergy. The influence of genetic factors has been shown by familial aggregation studies, and numerous candidate genes have been identified Gene polymorphisms interact with the environment, contributing to fetal programming Heritable epigenetic modifications occur rapidly in response to environmental factors and may explain the recent increase in food allergies and other atopic diseases. Atmospheric agents and the maternal diet during pregnancy may either increase or decrease the risk. Birth conditions, the intestinal microbiota, age at which food diversification begins, and exposure to food allergens and pollutants by inhalation, ingestion and skin contact may all contribute to the onset of food allergy in infancy. Partial prophylaxis is now within reach. Preventive information must be provided to families at high risk of atopy in their offspring.
食物过敏源于生理性胎儿Th2极化。在生命最初几个月向Th1优势的正常转变在特应性婴儿中存在缺陷。几个因素对食物过敏的发展至关重要。家族聚集性研究表明了遗传因素的影响,并且已经鉴定出许多候选基因。基因多态性与环境相互作用,促成胎儿编程。可遗传的表观遗传修饰会迅速响应环境因素发生,这可能解释了近期食物过敏和其他特应性疾病的增加。孕期的大气因素和母亲饮食可能增加或降低风险。出生条件、肠道微生物群、开始食物多样化的年龄以及通过吸入、摄入和皮肤接触暴露于食物过敏原和污染物,都可能导致婴儿期食物过敏的发生。现在部分预防已触手可及。必须向其后代有特应性高风险的家庭提供预防信息。