Serum cytokine levels in atopic dermatitis

Summary Elevated IgE responses and eosinophilia observed in patients with atopic dermatitis (AD) may reflect increased responses of type 2 T‐helper (Th2) cytokines with a concomitant decrease in interferon‐gamma (IFN‐γ) production. However, the cross‐regulation of Th1/Th2 derivation and function in...

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Veröffentlicht in:Clinical and experimental dermatology 2002-05, Vol.27 (3), p.225-229
Hauptverfasser: Yoshizawa, Y., Nomaguchi, H., Izaki, S., Kitamura, K.
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Sprache:eng
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Zusammenfassung:Summary Elevated IgE responses and eosinophilia observed in patients with atopic dermatitis (AD) may reflect increased responses of type 2 T‐helper (Th2) cytokines with a concomitant decrease in interferon‐gamma (IFN‐γ) production. However, the cross‐regulation of Th1/Th2 derivation and function in AD patients are incompletely characterized. Therefore, we investigated serum levels of several cytokines [interleukin (IL)‐18, IL‐12, IL‐10, IL‐2 and IFN‐γ] in patients with AD to assess their possible relationships to the severity of disease. Serum IL‐18 levels in AD patients were significantly higher than those in healthy controls [207 pg/mL; 95% confidence interval (CI), 172–242 pg/mL vs. 144 pg/mL; 95% CI, 116–178 pg/mL; P = 0.026]. Those IL‐18 levels significantly correlated with eosinophil counts and serum soluble IL‐2 receptor (sIL‐2R) levels, and showed a tendency to correlate with clinical severity scores and serum IgE levels. IL‐2 levels showed a significantly inverse correlation with serum IgE levels, and IL‐12 levels clearly correlated with IL‐10 levels. These results suggest the value of serum IL‐18 levels as a parameter of AD activity and may support a possible role for IL‐18 in the pathogenesis of AD. The inverse correlation between IgE levels and IL‐2 levels suggests that IgE production may be inhibited by IL‐2 in patients with AD. Furthermore, the correlation of IL‐12 levels with IL‐10 levels may support the previous reports that show the induction of IL‐10 production by human natural killer cells and/or T cells stimulated with IL‐12 in vitro.
ISSN:0307-6938
1365-2230
DOI:10.1046/j.1365-2230.2002.00987.x