Regulatory roles of IL-12, IL-4 and IFN-γ on IgE synthesis in atopic patients

Objective To investigate the mechanism of cytokine regulation in atopy by analyzing the effects of three major cytokines, IL-4, IL-12 and IFN-gamma on in vitro IgE synthesis of human peripheral blood mononuclear cell (PBMC) from normal individuals and atopic patients. Methods We investigated 5 normal individuals and 22 atopic patients including 12 allergic asthma, 8 allergic rhinitis and 2 atopic dermatitis. Human PBMCs were separated and incubated in 96-wells culture plates with different cytokines. Cultured for 7 days, the supernatant was collected and the contents of IgE synthesized in vitro were detected. Results There was no IgE synthesis in vitro of PBMC from all the normal individuals and 7 patients, however, of her 15 patients' PBMC could produce IgE in vitro. We found that rhIL-4 could induce in vitro IgE synthesis of PBMC from ail the normal individuals and 22 patients. rhIL-12 could inhibit IgE synthesis induced by rhIL-4. Further investigation of cytokine effects on IgE synthesis was conducted in 15 patients whose PBMCs did produce IgE in vitro (average level was 714 +/- 1105 ng/L). The following effects were observed: (1) 10 mu g/L rhIL-4 could augment in vitro IgE synthesis from 714 +/- 1105 ng/L to higher level of 1483 +/- 1396 ng/L; (2) 20 mu g/L rhIL-12 could inhibit in vitro IgE synthesis from 714 +/- 1105 ng/L to lower level of 452 +/- 969 ng/L; (3) rhIL-12 could block IgE synthesis induced by rhIL-4 to the level of 583 +/- 1084 ng/L; (4) 50 mu g/L IFN-gamma could inhibit in vitro IgE synthesis from 714 rt 1105 ng/L to the level of 461 +/- 1063 ng/L. Conclusions rhIL-4 could induce in vitro IgE synthesis, rhIFN-gamma could inhibit the in vitro IgE synthesis and rhIL-12 could antagonize rhIL-4 effect on in vitro IgE synthesis of PBMC from atopic patients.