The role of T cells and the effect of hydrocortisone on interleukin‐4‐induced IgE synthesis by non‐T cells

SUMMARY The role of T cells for IL‐4‐induced IgE synthesis by peripheral blood mononuclear cells (PBMC) was investigated. The removal of monocytes from PBMC abolished IL‐4‐induced IgE synthesis. When PBMC were separated into T and non‐T cells, non‐T cells alone were not able to secrete significant amounts of IgE in the presence ofIL‐4. Depending on the separation procedure, the reconstitution of non‐T cells with T cells prepared by rosetting did not restore IgE secretion, whereas T cells obtained by the use of anti‐CD3 antibodies could co‐induce IgE formation. However, when the T cells were first irradiated, large amounts of IgE were produced, which strongly exceeded those found in unscparated PBMC cultures. IL‐4‐induced IgE synthesis was also obtained in co‐cultures of formaldehyde‐fixed T cells with non‐T cells. Furthermore, not only autologous but also allogeneic T cells, which have been irradiated or fixed, could provide the costimulatory effect on IgE formation by non‐T cells in the presence of IL‐4. Mitogenically pre‐activated T cells, however, were not able to support IgE synthesis. Hydrocortisone (HC) potentiated the IL‐4‐induced IgE synthesis by PBMC and enabled non‐T cells to secrete IgE in the presence of IL‐4. Adding both HC and T cells led to a marked synergistic effect on IL‐4‐induced IgE production. We conclude that monocytes are required for the induction of IgE synthesis in PBMC in addition to T cells and IL‐4. Our results support the view that the T cell signal is delivered via cognate and non‐cognate T/B cell membrane interaction. Furthermore, active and proliferating T cells rather suppress IgE synthesis. Finally, HC appears to be a potent alternative stimulus, which bypasses the necessity for T cells in IL‐4‐induced IgE formation.