Abstract
The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on spontaneous IgE production was studied in B cells from atopic patients with allergic rhinitis, atopic eczema/dermatitis syndrome or bronchial asthma, and from non-atopic subjects. TCDD enhanced spontaneous IgE production in B cells from atopic patients without affecting production of IgG1, IgG2, IgG3, IgG4, IgM, IgA1 and IgA2, while TCDD failed to induce IgE production in B cells from non-atopic subjects. Purified surface IgE+(sIgE+) B cells from atopic patients spontaneously produced IgE, while surface IgE- (sIgE−) B cells failed to do so. TCDD enhanced spontaneous IgE production in sIgE+B cells, while TCDD with or without IL-4 or anti-CD40 mAb failed to induce IgE production in sIgE−B cells. Collectively, TCDD selectively enhanced ongoing IgE production. These results suggest that TCDD may aggravate allergic diseases by enhancing IgE-mediated allergic responses.
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