T cells from atopic individuals produce IgE‐inducing activity incompletely blocked by anti‐interleukin‐4 antibody

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Abstract
We investigated peripheral blood B and T lymphocyte functions in atopic individuals. B cells were co‐cultured with mutant EL4 thymoma cells in the presence of a standard T cell supernatant (T‐SN) with or without exogenous interleukin (IL)‐4. IgE secretion in this assay was found to be IL‐4 dependent, but not significantly different for atopic patients (n = 25) vs. normal controls (n = 25). Phytohemagglutinin plus phorbol 12‐myristate 13‐acetate (PHA+PMA)‐induced T‐SN from patients or controls was tested on normal B cells in the same assay system (in the absence of exogenous IL‐4). Compared to the controls, the IgE‐inducing activity was significantly increased for patients with asthma or allergic rhinitis (n = 12; p0.05). Since the assay was not inhibited by interferon (IFN)‐γ, this difference can not be attributed to IFN‐γ concentrations. Other T cell activities may be different between the patient groups or atopic T cells from the respiratory mucosa may recirculate more than those from the skin. In any case, the T cells rather than the B cells were found to be abnormal in atopic individuals.If atopic T cells were stimulated with PHA + PMA not as immediately but after a resting period of 48 h in culture medium alone, the IgE‐inducing activity, but not the total Ig‐inducing activity or the IL‐2 secretion, disappeared. In addition, a mean of 37 % of the IgE‐inducing activity (range of 13 % to 79 % for five very active T‐SN) was not inhibited by an anti‐IL‐4 antibody which neutralized exogenous IL‐4, indicating a participation of factors capable of bypassing the requirement for IL‐4 for the IgE response.