Skin Allergy

Introduction

Allergic 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 pro-inflammatory 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.

IgE-mediated skin disorders

Allergic skin pathology include disorders which are immunoglobulin E (IgE)-mediated, such as urticaria/angioedema, cell-mediated, such as contact dermatitis, or mediated by both these mechanisms, such as atopic dermatitis. While contact dermatitis is typically local, consisting in a skin inflammation in the site where contact with the hapten takes place, urticaria/angioedema (UA) and atopic dermatitis (AD) are systemic in their expression, as contact with the specific allergen in the gastrointestinal tract (as occurs for foods in both UA and AD) or the respiratory tract (as occurs for house dust mites in AD) is able to elicit an allergic reaction in the skin.

Urticaria/angioedema

The typical skin lesion of urticaria is the wheal, featured by a central swelling surrounded by erythema, associated with itching and generally receding after a few hours [1]. In angioedema the swelling is more pronounced, involves dermis and subcutis, is associated with pain more than itching, and has a slower resolution, requiring up to 72 h [1].

UA may be induced by a large number of causes, including physicochemical stimuli, infections, autoimmunity, vasculitis and others [2], and may have an acute (duration < 6 weeks) or chronic (> 6 weeks) presentation [1]. Allergy is a relatively frequent cause of acute UA, but accounts only for 5-10% of chronic UA [3]. The exposure to the specific allergen causes the release of mast cell mediators, with a prominent role for histamine [4]. In the case of local contact, as occurs for example with latex, urticaria may present at the site of contact (local urticaria), but most commonly the presentation is as generalized urticaria, which is elicited by the ingestion of the culprit food. It is of interest that in the oral allergy syndrome contact ...