The Modulation of Cytokine and IgE Production by Tumor Necrosis Factor-β in Atopic Dermatitis

SummaryAtopic dermatitis (AD) is associated with increased IL-4, IL-5, and IL-13 but decreased IFN-γ production. This cytokine profile may account for the atopic features of this illness, including IgE upregulation. Recent studies have demonstrated that tumor necrosis factor (TNF)-β is produced by Th1-like cells, but the cytokine modulation by TNF-β and the clinical significance of this cytokine in AD is not known. Therefore, this study was carried out to determine the potential role of TNF-β in AD. In this study, we cultured peripheral blood mononuclear cells from patients with AD and normal subjects with anti-CD3 monoclonal antibodies and investigated the production of TNF-β by ELISA. The mean ± SEM of TNF-β production in AD was significantly lower than normal subjects (p = 0.03). The effect of TNF-β on cytokine production was investigated by culturing peripheral blood mononuclear cells with anti-CD3 monoclonal antibodies in the presence or absence of TNF-β. Compared with medium control, TNF-β significantly decreased IL-5 (p = 0.0004) and IL-13 (p = 0.008) but increased IFN-γ (p = 0.001) production. The effect of TNF-β on IgE production was determined by culturing peripheral blood mononuclear cells in the IL-4- and anti-CD40-induced IgE production system. Interestingly, TNF-β significantly decreased IgE (p = 0.02), but not IgG production compared with medium control. Our study demonstrates that TNF-β production is downregulated in AD. This cytokine increases IFN-γ production but decreases IL-5, IL-13, as well as IgE production. These findings suggest a potential role for TNF-β in the pathogenesis of AD