Volume 124, Issue 4 , Pages 753-760.e1, October 2009
Expression of chemokines and chemokine receptors in lesional and nonlesional upper skin of patients with atopic dermatitis
Background
Trafficking of dendritic cell (DC) subtypes to and from the skin plays a pivotal role in atopic dermatitis (AD).
Objectives
We sought to determine the CCR pattern of epidermal DC subtypes and CCL expression in relation to the state of AD.
Methods
Shave biopsy specimens were taken from patients with AD before and after 24 and 72 hours of atopy patch testing and from the skin of patients with chronic AD, skin of patients with psoriasis, and healthy skin. CCR expression of epidermal DCs was studied by using flow cytometry, and chemokine mRNA levels in the skin were quantified by means of real-time PCR.
Results
The total number of CD1a+ epidermal DCs increased and the proportion of Langerin-positive CD1a+ DCs decreased whereas the percentage of Langerin-negative CD1a+ DCs increased after allergen application. Expression of CCR5 and CCR6 of Langerin-negative CD1a+ DCs was characteristic for acute AD. Expression of CCL1, CCL3, CCL4, and CCL11 mRNA was greater in patients with acute AD versus that seen in patients with chronic AD. Only a strong increase of CCLs, in particular CCL1, CCL17, and CCL18, went along with eczema development, and increased CCL1, CCL13, CCL17 and CCL18 expression was specific for patients with chronic AD compared with those with psoriasis.
Conclusion
Modified recruitment and differentiation of DCs from their dermal and blood precursors occurs in the acute phase of AD. A boost in the amplitude of CCLs after allergen application goes along with eczema development.
Key words: Dendritic cells, chemokines, chemokine receptors, atopic dermatitis, atopy patch test
Abbreviations used: AD, Atopic dermatitis, APT, Atopy patch test, DC, Dendritic cell, FITC, Fluorescein isothiocyanate, IDEC, Inflammatory dendritic epidermal cell, LC, Langerhans cell
Supported by grants from the Deutsche Forschungsgemeinschaft (DFG NO454/1-4; SFB704 TPA1, TPA4 and TPA15) and a BONFOR grant of the University of Bonn. N. N. is supported by a Heisenberg-Professorship of the DFG NO454/5-2.
Disclosure of potential conflict of interest: T. Bieber is a lecturer and consultant for Novartis, Astellas, Intendis, and Serono and receives research support from Astellas and Serono. I. Förster receives research support from Deutsche Forschungsgemeinschaft. N. Novak receives research support from the German Research Council and BONFOR and is a speaker for Astellas and Novartis. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(09)01009-4
doi:10.1016/j.jaci.2009.07.004
© 2009 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 124, Issue 4 , Pages 753-760.e1, October 2009
