Allergy and the skin

Abstract

SummaryAllergic skin disorders include urticaria, angioedema, contact dermatitis and atopic dermatitis, but the model fitting most closely the systemic concept of allergy is atopic dermatitis (AD), the pathogenesis of which is linked to a complex interaction between skin barrier dysfunction and environmental factors such as allergens and microbes. In particular, an important advance was the demonstration that the mutation of the skin barrier protein filaggrin is related strictly to allergen sensitization and to the development of asthma in subjects with AD. The altered skin barrier function, caused by several factors, results in the passage of allergens through the skin and to systemic responses. A pivotal role in such a response is exerted by Langerhans cells which, via their immunoglobulin E (IgE) receptor, capture the allergens and present them to T cells. When T helper type 2 (Th2) cells are activated, the production of a proinflammatory cytokines and chemokines pattern sustains the persistence of inflammation. Known AD-related cytokines are interleukin (IL)-5, IL-13 and tumour necrosis factor (TNF)-a, with emerging importance for IL-17, which seems to drive airway inflammation following cutaneous exposure to antigens, and IL-31, which is expressed primarily in skin-homing Th2 cells. Skin-homing is another crucial event in AD, mediated by the cutaneous lymphocyte-associated antigens (CLA) receptor, which characterizes T cell subpopulations with different roles in AD and asthma.

The mechanism of atopic march may be the ‘social’ event of cells and molecules (Review)

“…Urticaria and angioedema are wheals, characterized by central swelling surrounded by erythema, associated with itching. In the inflammatory process, both the dermis and the subcutis are involved, but the main target is the epidermis (30,34). AD is characterized by eczematous changes in the epidermis, and most patients have an atopic background with past or family histories of bronchial asthma, allergic rhinitis, and/or allergic conjunctivitis.…”

“…Infiltration of lymphoid cells into the epidermis and upper dermis can be observed under the microscope (34). The epidermal keratinocytes, which are triggers of immune abnormalities, as well as peripheral effectors, are important to further disclose the pathogenesis of this enigmatic disorder (29,30,34). Although the involved layer is different in individual cases of allergic skin diseases, the keratinocytes which produce cytokines and chemokines have been considered as the crucial factors in the initiation of skin inflammation (29,30,24).…”

“…Mast cells and IgE molecules may be intrinsically activated through allergen-mediated epithelial cells. Both bronchial asthma and AD are characterized by Th2-mediated chronic inflammatory diseases in response to allergen (7,9,32,34). Locally-produced but not circulating TSLP has been postulated to be a master regulator of Th2 inflammation with eosinophilia and hyper-IgE immunoglobulinemia (9).…”

“…Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Inflammation of the affected tissue is present in the epidermis and dermis where direct contact with the hapten takes place (34). Urticaria, angioedema, and AD are atopic disorders, in which contact of a specific allergen with the surface of the gastrointestinal or the respiratory tract drives an allergic reaction from the primary allergen contacted sites to the skin (30,34).…”

“…The skin may be the favorable and easiest observable organ for studying the pathogenesis of the systemic involvement of allergy, because during the allergic progress it always elicits an inflammatory reaction even though the primary allergen contact site is located in the skin, airways or digestive tract. Allergic skin disorders include urticaria, angioedema, contact dermatitis and atopic dermatitis (AD) (34). Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance.…”