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Phenotyping of epidermal dendritic cells allows the differentiation between extrinsic and intrinsic forms of atopic dermatitis
Author(s) -
Oppel T.,
Schuller E.,
Günther S.,
Moderer M.,
Haberstok J.,
Bieber T.,
Wollenberg A.
Publication year - 2000
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2000.03887.x
Subject(s) - atopic dermatitis , immunology , immunoglobulin e , dendritic cell , pathogenesis , langerhans cell , allergy , medicine , antigen , antibody
Atopic dermatitis (AD) is a clinically characteristic, chronic inflammatory skin disease of unknown origin. IgE‐mediated uptake and antigen focusing of environmental allergens by dendritic cells (DCs) is assumed to be a central immunopathogenetic event. A so‐called intrinsic type of AD (IAD) has been delineated from the more common extrinsic AD (EAD) by normal serum IgE levels, negative RAST tests and negative immediate‐type skin reactions towards environmental allergens. The recently characterized human autoantigen Hom S 1 has been proposed to play a part in the pathogenesis of IAD. Objectives To compare clinical and laboratory data between patients with IAD and EAD, and to investigate potential differences in the inflammatory micromilieu of the epidermal compartment in IAD and EAD lesions. Methods Epidermal DC phenotyping, a recently validated technique based on the three‐colour flow cytometric analysis of Langerhans cells and the so‐called inflammatory dendritic epidermal cells from epidermal single‐cell suspensions, was performed on samples from 69 patients with AD (seven with IAD and 62 with EAD) and 94 controls. Results Patients with EAD tended to have an earlier onset of disease but similar disease duration and family history of atopic diseases. Quantitative analysis of CD36 expression on DCs as a marker of inflammation, as well as the percentage of inflammatory dendritic epidermal cells in the CD1a+ epidermal DC pool, indicated a comparable disease activity in IAD and EAD. EAD was characterized by a significantly higher FcεRI expression on the CD1a+ epidermal DCs than IAD. Using the FcεRI/FcγRII expression ratio as a disease marker for AD, values for IAD fell below the diagnostic cut‐off level of 1·5 for this ratio. Conclusions While IAD is clinically similar to EAD, the inflammatory microenvironment in this condition seems different from classical EAD and can be distinguished by phenotyping of epidermal DCs.