Abnormal regulation of in vitro IgE synthesis by T cells obtained from patients with atopic dermatitis.

The regulatory influence of atopic eczema and non-atopic T cells on spontaneous IgE synthesis by eczema B cells was examined. Eczema B cells were cocultured with either autologous or allogeneic T cells in RPMI 1640 with 10% fetal calf serum at 0.75 X 10(6) cells/ml (B/T = 0.5) and supernatant IgE was measured by a modified PRIST assay. Net IgE synthesis was obtained by subtracting preformed IgE (+ cycloheximide at Day 0) from total IgE in 7-day supernatants. T cells were either untreated, heat-killed, exposed to 2000 rad, or depleted of helper/suppressor T cells by "panning" with monoclonal antibodies (Leu 3a and Leu 2a). Atopic eczema B cells spontaneously synthesized IgE when cultured alone. No significant suppression of net IgE synthesis occurred when atopic eczema T cells were cocultured with autologous B cells. In allogeneic recombinations, non-atopic T cells significantly suppressed net IgE synthesis by atopic eczema B cells (mean suppression = 59%; P less than 0.05). This suppression was abrogated if allogeneic control T cells were heat-killed, irradiated, or depleted of Leu 2a+ suppressor cells. In order to exclude an "allogeneic effect" as the sole mechanism to explain the suppression of IgE synthesis observed by coculturing non-atopic T cells with eczema B cells, the latter were recombined with either T cells from HLA-DR and mixed lymphocyte culture-matched sibling or autologous T cells. Greater suppression of net IgE synthesis was seen in the presence of histoidentical non-atopic T cells than in the presence of autologous eczema T cells, indicating that the latter have a partial defect in their suppressor function. This apparent "defect" in immunoregulatory function may be overcome by in vitro activation of atopic eczema T cells by concanavalin A.