The epithelial barrier is a critical defense mechanism that separates the human body from the external environment, performing both physical and immune functions. It plays a vital role in protecting the body from environmental risk factors such as allergens, pathogens, and pollutants. However, since the 19th century, environmental pollution, global warming, increased use of industrial chemicals, and changes in biodiversity have led to a significant rise in allergic disease incidence. Allergic diseases frequently exhibit dysfunction in the epithelial barrier. The epithelial barrier hypothesis proposes a new approach for the prevention and treatment of allergic diseases. Despite increased attention to the role of barrier dysfunction in allergic disease development, many questions remain about the mechanisms underlying the disruption of normal barrier function. This review aims to provide a comprehensive overview of the epithelial barrier's role in allergic diseases, including influencing factors, assessment techniques, and repair methods. By doing so, it seeks to present innovative strategies for the prevention and treatment of allergic diseases. Keywords: epithelial barrier, allergic diseases, barrier dysfunction, type 2 inflammation, prevention and treatment The epithelial barrier is composed of tight junctions (TJs), adherens junctions (AJs), and desmosomes. TJ complex includes claudins, occludins, and junctional adhesion molecules, with major cytoplasmic proteins including ZO-1, ZO-2, and ZO-3. AJs, positioned directly below the TJ, encompass E-cadherin, actin, vinculin, α-catenin, and β-catenin. Desmosomes, characterized by a symmetrical structure involving two adjacent plasma membranes, play a vital role in establishing and maintaining stable cellular junctions. Epithelial barrier dysfunction is a common pathway contributing to the initiation and exacerbation of allergic diseases. Research has established the involvement of the epithelial barrier in the pathological progression of allergic diseases. Dysfunction in the epithelial barrier across various human tissues is characterized by cell differentiation, compromised junction integrity, and impaired innate defenses. Genetic predisposition, environmental influences, and aberrant inflammation collectively promote the dysfunction and breakdown of the epithelial barrier, precipitating the onset and progression of allergic diseases. Studies indicate that compromised epithelial barriers activate epithelial cells, leading to the release of alarm factors such as interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP). This, in turn, promotes cytokine release by type 2 innate immune cells, triggering and exacerbating type 2 immune responses. Epithelial barrier dysfunction is closely linked to the development of allergic diseases such as asthma, allergic rhinitis (AR), atopic dermatitis (AD), and food allergy (FA). In asthma, the airway epithelial barrier is crucial for maintaining the host's health. Prolonged exposure to external stimuli can lead to the manifestation of epithelial barrier dysfunctionThe epithelial barrier is a critical defense mechanism that separates the human body from the external environment, performing both physical and immune functions. It plays a vital role in protecting the body from environmental risk factors such as allergens, pathogens, and pollutants. However, since the 19th century, environmental pollution, global warming, increased use of industrial chemicals, and changes in biodiversity have led to a significant rise in allergic disease incidence. Allergic diseases frequently exhibit dysfunction in the epithelial barrier. The epithelial barrier hypothesis proposes a new approach for the prevention and treatment of allergic diseases. Despite increased attention to the role of barrier dysfunction in allergic disease development, many questions remain about the mechanisms underlying the disruption of normal barrier function. This review aims to provide a comprehensive overview of the epithelial barrier's role in allergic diseases, including influencing factors, assessment techniques, and repair methods. By doing so, it seeks to present innovative strategies for the prevention and treatment of allergic diseases. Keywords: epithelial barrier, allergic diseases, barrier dysfunction, type 2 inflammation, prevention and treatment The epithelial barrier is composed of tight junctions (TJs), adherens junctions (AJs), and desmosomes. TJ complex includes claudins, occludins, and junctional adhesion molecules, with major cytoplasmic proteins including ZO-1, ZO-2, and ZO-3. AJs, positioned directly below the TJ, encompass E-cadherin, actin, vinculin, α-catenin, and β-catenin. Desmosomes, characterized by a symmetrical structure involving two adjacent plasma membranes, play a vital role in establishing and maintaining stable cellular junctions. Epithelial barrier dysfunction is a common pathway contributing to the initiation and exacerbation of allergic diseases. Research has established the involvement of the epithelial barrier in the pathological progression of allergic diseases. Dysfunction in the epithelial barrier across various human tissues is characterized by cell differentiation, compromised junction integrity, and impaired innate defenses. Genetic predisposition, environmental influences, and aberrant inflammation collectively promote the dysfunction and breakdown of the epithelial barrier, precipitating the onset and progression of allergic diseases. Studies indicate that compromised epithelial barriers activate epithelial cells, leading to the release of alarm factors such as interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP). This, in turn, promotes cytokine release by type 2 innate immune cells, triggering and exacerbating type 2 immune responses. Epithelial barrier dysfunction is closely linked to the development of allergic diseases such as asthma, allergic rhinitis (AR), atopic dermatitis (AD), and food allergy (FA). In asthma, the airway epithelial barrier is crucial for maintaining the host's health. Prolonged exposure to external stimuli can lead to the manifestation of epithelial barrier dysfunction