Since the 1970s, the number of patients with allergic diseases has surged, and it is now estimated that about half of the population suffers from some form of allergic condition, making it a significant social issue. Allergic diseases are considered “multifactorial diseases” caused by a complex interplay of genetic predisposition and environmental factors. However, since genetic predisposition is unlikely to change dramatically in a short period, the rapid increase in the number of patients in such a short time is mainly attributed to environmental changes.

The most well-known hypothesis explaining the increase in allergic diseases is the “hygiene hypothesis.” Based on various epidemiological studies, this theory suggests that as environments became more hygienic with modernization, the opportunities for exposure to microorganisms (bacteria and viruses) during early childhood decreased, leading to an increase in allergies. This hypothesis is widely accepted today. In recent years, however, the “epithelial barrier hypothesis” has been proposed, suggesting that the dysfunction of the barrier function of epithelial cells, which are present in the parts of the body that interact with the external environment, due to various external and internal factors, leads to the onset of allergic diseases.

In this presentation, I will focus on environmental factors and the epithelial cells exposed to them, introducing the mechanisms that trigger allergic inflammation. Additionally, it has been suggested that among allergic diseases traditionally considered “multifactorial,” some severe cases may actually be “monogenic diseases” caused by abnormalities in a single gene. I will also introduce the latest findings on genetic abnormalities that can cause allergic diseases and their neuro-immune regulation.

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