Soluble CD30 is more relevant to disease activity of atopic dermatitis than soluble CD26

It is suggested that CD30 and CD26 are surface molecules expressed on activated Th2 and Th1 cells, respectively. We examined plasma levels of soluble CD26 (sCD26) and sCD30 in patients with atopic dermatitis (AD) when their eruptions were aggravated and in non‐atopic healthy controls, and then analy...

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Published in:Clinical and experimental immunology Vol. 121; no. 2; pp. 187 - 192
Main Authors: Katoh, N., Hirano, S., Suehiro, M., Ikenaga, K., Yamashita, T., Sugawara, N., Yasuno, H.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Science Ltd 01-08-2000
Blackwell
Oxford University Press
Blackwell Science Inc
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Summary:It is suggested that CD30 and CD26 are surface molecules expressed on activated Th2 and Th1 cells, respectively. We examined plasma levels of soluble CD26 (sCD26) and sCD30 in patients with atopic dermatitis (AD) when their eruptions were aggravated and in non‐atopic healthy controls, and then analysed the possible correlation between these values and the levels of several clinical markers. The plasma levels of both sCD30 and sCD26 were significantly higher in AD patients than in controls, both in exacerbation status and after conventional treatment. Multiple regression analyses showed that plasma sCD30 was a much better predictor of the levels of serum IgE, serum LDH and plasma sCD25, and the area and the score of AD eruption than sCD26, although elevated levels of both sCD30 and sCD26 are associated with these clinical predictors of AD. Importantly, sCD30 plasma levels decreased significantly in AD patients after conventional treatment, while no significant transition was noted in the concentration of sCD26. Moreover, a significant reduction of sCD30 levels was observed in the group of patients whose eruption score was reduced > 50%, whereas it was not in those < 50%. These findings provide evidence that the successful treatment of AD is associated with down‐activation of Th2.
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ISSN:0009-9104
1365-2249
DOI:10.1046/j.1365-2249.2000.01286.x