The hygiene hypothesis has been popularized as an explanation for the rapid increase in allergic disease observed over the past 50 years. Subsequent epidemiological studies have described the protective effects that in utero and early life exposures to an environment high in microbial diversity have in conferring protective benefits against the development of allergic diseases. The rapid advancement in next generation sequencing technology has allowed for analysis of the diverse nature of microbial communities present in the barrier organs and a determination of their role in the induction of allergic disease. Here, we discuss the recent literature describing how colonization of barrier organs during early life by the microbiota influences the development of the adaptive immune system. In parallel, mechanistic studies have delivered insight into the pathogenesis of disease, by demonstrating the comparative effects of protective T regulatory (Treg) cells, with inflammatory T helper 2 (Th2) cells in the development of immune tolerance or induction of an allergic response. More recently, a significant advancement in our understanding into how interactions between the adaptive immune system and microbially derived factors play a central role in the development of allergic disease has emerged. Providing a deeper understanding of the symbiotic relationship between our microbiome and immune system, which explains key observations made by the hygiene hypothesis. By studying how perturbations that drive dysbiosis of the microbiome can cause allergic disease, we stand to benefit by delineating the protective versus pathogenic aspects of human interactions with our microbial companions, allowing us to better harness the use of microbial agents in the design of novel prophylactic and therapeutic strategies.

作为对过去 50 年来观察到的过敏性疾病迅速增加的解释，卫生学假说已得到普及。随后的流行病学研究描述了在子宫内和生命早期暴露于微生物多样性高的环境中对预防过敏性疾病的预防作用。下一代测序技术的快速进步使得能够分析屏障器官中存在的微生物群落的多样性，并确定它们在诱发过敏性疾病中的作用。在这里，我们讨论最近的文献，这些文献描述了微生物群在生命早期对屏障器官的定植如何影响适应性免疫系统的发展。在平行下，机制研究通过证明保护性调节性 T 细胞 (Treg) 与炎症辅助性 T 2 (Th2) 细胞在发展免疫耐受或诱导过敏反应方面的比较作用，深入了解了疾病的发病机制。最近，我们对适应性免疫系统和微生物衍生因素之间的相互作用如何在过敏性疾病的发展中发挥核心作用的理解取得了重大进展。更深入地了解我们的微生物组和免疫系统之间的共生关系，这解释了卫生假说的关键观察结果。通过研究导致微生物群失调的扰动如何导致过敏性疾病，