Abstract
An epicutaneous patch test with allergens known to elicit IgE-mediated reactions and the evaluation of eczematous skin lesions after 24 h to 72 h is called the atopy patch test (APT) [1]. This test was developed as a diagnostic tool for characterizing patients with aeroallergen-triggered atopic eczema (AE, atopic dermatitis), a chronic inflammatory skin disease. AE is characterized by a combination of clinical features, including pruritus and a typically age-related distribution and skin morphology [2, 3]. Patients with AE often have elevated serum levels of immunoglobulin E (IgE), often directed against aeroallergens (e.g., house dust mites) and food allergens. These allergens produce flares in some patients with AE,but not in all sensitized individuals [4]. Also, aeroallergen avoidance, especially with regard to house dust mites, can result in marked improvement of skin lesions [5]. Among the allergens found to be relevant in AE, aeroallergens and food allergens (in children) are the most important. Therapeutic consequences of the diagnosis of allergy are based upon avoidance strategies, thus, the relevance of (often multiple) IgE-mediated sensitizations in patients with AE for the skin disease has to be evaluated. In spite of these clinical aspects, the role of allergy in eliciting and maintaining the eczematous skin lesions was controversial [6], partially due to a lack of specificity of the classic tests for IgE-mediated hypersensitivity, skin prick test, and measurement of specific serum IgE. Mite allergen in the epidermis of patients with AE under natural conditions [7], as well as in APT sites [8, 9], has been demonstrated in proximity to Langerhans cells. Langerhans cells in the skin express IgE receptors of three different classes [1012]. In addition, a Birbeck-granule-negative, non-Langerhanscell population with an even higher IgE receptor expression than the Langerhans cell, the so-called inflammatory dendritic epidermal cells (IDEC) [13], has recently been demonstrated in freshly induced APT lesions, a phenomenon which occurred in both "intrinsic" and "extrinsic" patients [14]. This might explain the IgE-associated activation of allergen-specific T-cells, leading finally to eczematous skin lesions in the APT (Fig. 1) [15, 16].According to the results of Langeveld-Wildschut et al., the positive APT reaction requires the presence of epidermal IgE+ CD1a+ cells [17]. From APT biopsies, allergen-specific T-cells have been cloned [16]. These T-cells showed a characteristic TH2 (T helper cell subpopulation) secretion pattern initially, whereas, after 48 h, a TH1 pattern was predominant. This same pattern is also found in chronic lesions of AE.
| Original language | English |
|---|---|
| Title of host publication | Contact Dermatitis |
| Publisher | Springer Berlin Heidelberg |
| Pages | 391-399 |
| Number of pages | 9 |
| ISBN (Print) | 3540244719, 9783642038266 |
| DOIs | |
| State | Published - 2011 |