Atopic dermatitis is regarded as mediated by Th2-type immunity. In fact, it frequently coincides with the elevation of
immunoglobulin (Ig)-E in patients' sera. Due to the pivotal role of
interleukin (IL)-4 in regulation of
IgE, we hypothesized if
atopic dermatitis represents a hyper-reactive condition in response to
IL-4 when it coincides the higher serum level of
IgE. To address this possibility, peripheral blood mononuclear cells (PBMC) isolated from patients with
atopic dermatitis with the high serum
IgE level, from those with
psoriasis or from healthy volunteers were stimulated with recombinant
IL-4 and analyzed for activation of
transcription factors including activator
protein (AP)-1 or signal transducers and activators of transcription (STAT)-6 by employing electrophoretic mobility shift assays. Although no significant difference between atopy patients and other groups was observed in the STAT-6 binding activity in IL-4-stimulated PBMC, it over-activated the binding of
AP-1 in PBMC of the patients with
atopic dermatitis. The
AP-1 binding was interfered by the use of an antibody directed against JunB. This is the indication that IL-4-overactivated
AP-1 is composed of JunB. Furthermore, semi-quantitative RT-PCR analyses revealed marked down-modulation of a Th1
cytokine,
interferon (IFN)-gamma, in IL-4-stimulated PBMC derived from atopy patients, but not that from healthy individuals. Together, our present study indicates that
AP-1 is over-activated by
IL-4 in PBMC of the atopic patients with the higher
IgE level, thereby implying that IL-4-induced over-activation of
AP-1 might be one of pathogenic factors in
atopic dermatitis.