BASOPHIL HISTAMINE-RELEASE AND LEUKOTRIENE PRODUCTION IN RESPONSE TO ANTI-IGE AND ANTI-IGE RECEPTOR ANTIBODIES - COMPARISON OF NORMAL SUBJECTS AND PATIENTS WITH URTICARIA, ATOPIC-DERMATITIS OR BRONCHIAL-ASTHMA

The IgE receptor-dependent in vitro mediator release in basophils is c haracterized by a large interindividual variability both in normal and atopic subjects. The mechanism and the clinical impact of this findin g, however, is largely unclear. The aim of the present study was to ex amine the role of surface-bound IgE and of response-modifying cytokine s such as interleukin 3 (IL-3) as possible factors determining basophi l releasability in atopic patients and normal controls. Cells from 30 individuals (6 with urticaria, 7 with asthma, 7 with atopic dermatitis , and 30 healthy controls) were isolated and stimulated for mediator r elease by IL-3 and different triggering antibodies directed against Ig E or IgE receptor. Our data suggest that serum IgE levels and basophil receptor occupancy with IgE are not involved in the mechanism of baso phil releasability. Furthermore, IL-3-induced similar effects on media tor release in almost all individuals, rather excluding the possibilit y that releasability is regulated by cytokine priming of basophils. In terestingly, we found that patients with atopic disease have a reduced capacity of releasing mediators upon activation, the mechanism of whi ch is unclear. In conclusion, our findings support the hypothesis that basophil releasability is dependent on cell-immanent mechanisms in ba sophils, which may be altered in selected atopic patients.