1. ^*Asthma and Allergic Diseases Center, Department of Internal Medicine, Charlottesville, Virginia, USA
2. ^†Department of Dermatology, University of Virginia, Charlottesville, Virginia, USA
3. ^‡Department of Genomics and Informations Sciences, Hoffman-La Roche, Nutley, New Jersey, USA

Correspondence: Dr Judith Woodfolk, Asthma and Allergic Diseases Center, University Health System, PO Box 801355, Charlottesville, VA 22908-1355, USA Email: jaw4m@virginia.edu

Received 23 May 2003; Revised 22 October 2003; Accepted 4 November 2003.

Abstract

Atopic dermatitis (AD) is often associated with high titer IgE antibodies (ab) to allergens, and IL-10-mediated regulation of IFN- has been proposed to contribute to this IgE ab production. However, the relevance of IL-10 and IFN- to IgE associated with AD has not been examined in the context of an allergen-specific system. Analysis of PBMC responses in vitro showed deficient T cell proliferation to overlapping IL-10- (peptide (P) 2:1) and IFN-- (P2:2) inducing chain 2 major epitopes of cat allergen (Fel d 1) in cultures from sensitized AD patients (mean IgE to cat=20.9 IU/ml). Diminished IFN- induction by Fel d 1 and P2:2, along with elevated peptide-induced IL-10 (except for P2:1) was observed in PBMC cultures from AD subjects compared with non-AD (sensitized and non-sensitized) subjects. Neither T cell proliferation nor IFN- production to chain 2 epitopes could be restored by anti-IL-10 mAb in cultures from sensitized AD subjects. Moreover, allergen avoidance was associated with a paradoxical decrease in both IL-10 and IFN- in peptide-stimulated PBMC from these subjects. Control of IFN- production to chain 2 epitopes by IL-10 may be relevant to sensitization status. Development of high titer IgE ab in AD could reflect a failure of this mechanism.