Abstract
Atopic dermatitis (AD) patients mount IgE antibody responses to a variety of environmental allergens and also to autoantigens. We analyzed serum samples from four AD patients who had received oral cyclosporine A (CyA) treatment for up to 17 months regarding IgE autoreactivity to nitrocellulose‐blotted human epithelial cell extracts and IgE levels to environmental allergens by quantitative ImmunoCap measurements. Skin inflammation was assessed by SCORAD. During full‐dose treatment, a strong reduction in T‐cell‐mediated skin symptoms was observed which reappeared when CyA treatment was reduced or stopped. The intensity of IgE autoreactivity seemed to follow skin inflammation as it was reduced during full‐dose treatment and increased upon inflammation. Interestingly, IgE levels to exogenous allergens were boosted by allergen exposure, declined thereafter, and seemed to be unaffected by CyA. Our data thus indicate that allergen‐specific IgE production is boosted by allergen contact and cannot be reduced by CyA‐mediated T‐cell suppression.
Highlights
Type I allergy is an IgE-mediated hypersensitivity disease affecting almost 25% of the population in industrialized countries [1]
Systemic cyclosporine A (CyA) treatment improves skin symptoms in Atopic dermatitis (AD) patients which is accompanied by a reduction in IgE autoreactivity
IgE autoreactivity to a 70-kDa and 21-kDa band became weaker after treatment was started and appeared again when the SCORAD rose between March and September 1995 and in the end of the treatment in patient 2 (Fig. 2B, C)
Summary
Type I allergy is an IgE-mediated hypersensitivity disease affecting almost 25% of the population in industrialized countries [1]. IgE reactivity profiles in adult allergic patients remain stable and only allergen-specific IgE levels change depending on allergen exposure [6, 7]. Evidence has been provided that the secondary IgE production in sensitized allergic subjects or animals does not require T-cell help. It has been demonstrated that primary allergic sensitization can be prevented by co-stimulation blockade, whereas secondary IgE production is not affected in a murine model of grass pollen allergy [8]. It has been shown that only intact, IgE-reactive allergens but not T-cell epitope-containing, non-IgE-reactive allergen fragments boost secondary IgE production in allergic patients [9]. We had the opportunity to investigate the effects of treatment with systemic cyclosporine A, a T-celltargeting drug on allergen-specific IgE production. Sera from patients with atopic dermatitis who had received systemic CyA treatment for up to 17 months were studied regarding
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