4.7 Article

Atopy patch test reactions show a rapid influx of inflammatory dendritic epidermal cells in patients with extrinsic atopic dermatitis and patients with intrinsic atopic dermatitis

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 111, Issue 4, Pages 869-874

Publisher

MOSBY, INC
DOI: 10.1067/mai.2003.1347

Keywords

atopic dermatitis; Langerhans cells; inflammatory dendritic epidermal cells; atopy patch test

Ask authors/readers for more resources

Background: Normal human skin harbors a single epidermal dendritic cell (DC) population, the CD1a(.+++)CD11b(-) Langerhans cells. In many chronic inflammatory skin diseases, the epidermal DC pool bears a second population, the CD1a(+)CD11b(+++) inflammatory dendritic epidermal cells (IDECs). Immunophenotypic, ultrastructural, and functional aspects of IDECs have been investigated in chronic untreated skin lesions of intrinsic and extrinsic atopic dermatitis (AD), contact dermatitis (CD), and psoriasis, but little is known about freshly induced early skin lesions. Objective: We sought to characterize enumerative and immunophenotypic changes in the epidermal DC pool during the development of eczematous skin lesions. Methods: The atopy patch test with aeroallergens and food-protein allergens and a conventional patch test with standard-series haptens were performed as models for early skin lesions of extrinsic and intrinsic AD and CD, respectively. After 72 hours, epidermal cell suspensions were prepared, analyzed in a standardized flow cytometric technique, and compared with the results obtained from chronic lesions. Results: The migration of IDECs into the epidermis occurs within 72 hours and is thus an early event. It continues in chronic AD, but not in chronic CD, lesions. The specific upregulation of FcepsilonRI, especially on IDECs, occurs later during formation of extrinsic but not intrinsic AD lesions. LCs were negative for CD36 in patch test lesions, whereas in chronic skin lesions, LCs expressed CD36. Conclusion: The DC alteration during skin lesion formation can be subdivided into early and late events, with the influx of IDECs as an early event and the alteration of the DC phenotype as a late event.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available