Serum thymus and activation-regulated chemokine, macrophage-derived chemokine and eotaxin as markers of severity of atopic dermatitis

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Abstract:

Background: 

Expression of CCR4 ligands, such as thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC), leads to preferential influx of T-helper (Th) 2-type lymphocytes to the lesional skin in atopic dermatitis (AD). Eotaxin, like the CCR3 ligand, is an important contributor of eosinophils recruitment in the course of AD. These chemokines are assumed to play an important role in the patomechanism of AD. Methods: 

In this study, the serum concentration of TARC, MDC, eotaxin and total immunoglobulin E (IgE) in AD patients and healthy people were compared. Correlation between the studied indices and activity of AD was established. Severity of AD was assessed according to the SCORAD score. The study comprised 44 healthy people and 43 patients with AD. The serum concentrations of TARC, MDC, eotaxin and IgE were measured with the use of enzyme-linked immunosorbent assay kits. Results: 

The serum levels of TARC, MDC, eotaxin and IgE appeared to be significantly higher in patients with AD than in healthy people. A strong positive correlation was revealed between the levels of TARC, MDC, total IgE in serum of patients with AD and SCORAD. In contrast, no significant relationship was found for the serum eotaxin concentration and TARC, MDC, IgE or disease severity. Conclusion: 

Our findings indicate that TARC and MDC are actively involved in the pathogenesis of AD and their expression, opposite to that of eotaxin, is strongly associated with clinical picture of atopic dermatitis.

Keywords: atopic dermatitis; macrophage-derived chemokine; thymus and activation-regulated chemokine

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1398-9995.2005.00774.x

Affiliations: 1: Department of Internal Medicine, Pneumonology and Allergology 2: Department of Dermatology, Central Hospital of Military Institute of Medicine, Warsaw, Poland

Publication date: May 1, 2005

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