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Cyclosporin A (CyA) reduces sCD30 serum levels in atopic dermatitis: a possible new immune intervention
Author(s) -
Bottari V,
Frezzolini A,
Ruffelli M,
Puddu P,
De Pità O,
Fontana L
Publication year - 1999
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.1999.00958.x
Subject(s) - atopic dermatitis , medicine , pathogenesis , immunology , allergy , immune system , asthma , food allergy , interleukin , cytokine
Atopic dermatitis (AD) is a chronic inflammatory skin disease frequently associated with asthma, rhinitis, and food allergy. Lymphocytes producing Th2‐type cytokines (such as interleukin [IL]‐3, IL‐4, and IL‐5) have been thought to have a key role in the pathogenesis of the disease. We have recently demonstrated that elevated serum levels of the soluble form of CD30 (sCD30), an activation marker of Th2‐cell clones, correlates with disease activity in pediatric patients suffering from AD. Clinical trials have demonstrated that cyclosporin A (CyA) treatment resulted in significant improvement of clinical symptoms in patients affected with AD. In this study, we evaluated the role of CyA in modulating sCD30 release in a group of adult patients affected by severe AD treated with CyA at the dosage of 3.5 mg/kg body weight for 12 weeks. Our results demonstrated, in parallel with an improvement of clinical symptoms, a significant reduction of serum levels of both IL‐4 and sCD30, thus suggesting that CyA can prevent the activation of Th2 cells observed in AD.