Allergy as an epithelial barrier disease

Acute allergic reactions are known to be symptomatic type-I hypersensitivity responses caused by an allergen cross-linking specifically with anti-IgE molecules on the surface of pre-sensitized mast cells [1-4]. In Europe the incidence of allergies rapidly increasing and thus we are facing an epidemic outburst of these diseases [5]. Even though costs per a patient are usually small allergies cause a major economical burden to the society, since up to 20% of the population now suffers from these disorders for instance in Finland [6]. Because of this the Finnish authorities have launched an "Allergy project 2008-2018", where a new direction has been taken. Here the patients will now be tolerated towards the antigens instead of avoiding them [6].Currently there are two, partially different basic theories on the pathogenesis of allergy. For decades the primary assumption has been that allergy is caused by unbalanced and overactive immunological responses against allergens, mostly driven by activated Th2 cells and due to aberrant T- regulatory cells. The second more recent hypothesis relies on the dysregulation of the epithelial barrier, which might result in the allergen uptake as a primary defect in the pathogenesis of allergic reactions. There is a wealth of literature on T cell responses in allergic diseases [7,8], and thus the objective of this review is to focus on putative modified epithelial functions related to allergy [9-11].Respiratory epithelium is the first barrier to the external environment and thus crucially important in the protection of the internal environment. Normally three independent and complex networks connect epithelial cells to each other; desmosomes, adherens junctions, and tight junctions [12]. The respiratory epithelium senses changes in its local environment such as the allergen exposure and also actively responds to these changes [13,14].Interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP) are cytokines, which have a role in