Abstract
The immunopathogenic role of house dust mite (HDM) allergens in the development of skin lesions in atopic dermatitis (AD) has not yet been precisely clarified. We immunohistopathologically evaluated the localization of immunoglobulin E (IgE)-positive epidermal dendritic cells with HDM antigens in the skin lesions of patients with IgE-allergic AD. Using double-immunofluorescence and single-immunochemical staining methods, we analyzed biopsy specimens from the skin lesions of six patients with IgE-allergic AD and HDM allergy and 11 control subjects with inflammatory skin disorders. Inflammatory dendritic epidermal cells (IDECs; CD11c+ and CD206+ cells) were markedly observed in the central area of the spongiotic epidermis of skin lesions in all AD patients. Furthermore, IgE-positive IDECs with HDM antigens in the central areas of the spongiosis were found in four of the six (66.7%) AD patients. Langerhans cells (LCs; CD207+ cells) with HDM antigens were also observed in the peripheral areas of the spongiosis. Infiltration of CD4+ and CD8+ T cells in association with IgE-positive IDECs and LCs with HDM antigens was seen in the spongiotic epidermis. An IgE-mediated delayed-type hypersensitivity reaction, in combination with IgE-bearing dendritic cells, specific T cells, keratinocytes, and HDM antigens, may lead to spongiotic tissue formation in eczematous dermatitis in AD.
Highlights
The pathophysiology of atopic dermatitis (AD) is complex, its basic axis is considered to be T cell-mediated immune reactions in association with immunoglobulin (Ig)E-type hypersensitivity specific to environmental exposures, such as to aeroallergens and food allergens [1,2,3]
CD8+ T cells in association with immunoglobulin E (IgE)-positive inflammatory dendritic epidermal cells (IDECs) and Langerhans cells (LCs) with house dust mite (HDM) antigens was seen in the spongiotic epidermis
We performed statistical comparisons mainly for the items associated with AD subjects and the control subjects with non-eczematous inflammatory skin disorders and serum hyper-IgE, since the present study primarily focused on the role of IgEs against HDM antigens
Summary
The pathophysiology of atopic dermatitis (AD) is complex, its basic axis is considered to be T cell-mediated immune reactions in association with immunoglobulin (Ig)E-type hypersensitivity specific to environmental exposures, such as to aeroallergens and food allergens [1,2,3]. Epidermal and dermal dendritic cells (DCs), such as Langerhans cells (LCs), inflammatory dendritic epidermal cells (IDECs), and dermal inflammatory DCs, are thought to be the principal antigen-presenting cells and potential sources of inflammatory mediators in AD that initiate and sustain the cellular infiltration of allergen-specific. LCs are defined as epidermal DCs that contain Birbeck granules and mainly express cluster of differentiation (CD)1a and CD207. IDECs are defined as epidermal inflammatory DCs that do not contain. Birbeck granules and mainly express CD1a, CD11b, CD11c, and CD206 antigens [4,5]. Dermal inflammatory DCs (so-called atopic DCs) that upregulate T helper (Th)2-attracting chemokines (e.g., thymus and activation-regulated chemokine (TARC)/CC Chemokine. Ligand (CCL) 17) express CD11c antigens [5].
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