IgE-mediated basophil releasability is influenced by intrinsic factors and by IgE on the cell surface.

Experiments were done to clarify the mechanisms associated with releasability of histamine. First, washed leukocytes from 23 asthmatic patients sensitive to mite allergen were challenged with Der p 1, a major allergen isolated from Dermatophagoides pteronyssinus, or anti-IgE. A significant correlation was observed between the ratio of Der p 1-specific IgE titer to total IgE level (S/T) in the patient's plasma and either the reactivity (maximal percentage of histamine release; rs = 0.514, P = 0.016, n = 23) or the sensitivity (the minimum allergen concentration required to achieve 25% histamine release; rs = -0.790, P = 0.0002) to Der p 1. Additionally, the reactivity to Der p 1 was significantly correlated with that to anti-IgE (rs = 0.690, P = 0.0012), indicating that an intrinsic cellular property may be one of the contributing factors in immunologic histamine release. In a second series of experiments, sinus mast cells were passively sensitized with immunoglobulins prepared from the patient's plasma. A statistically significant correlation was found between either the reactivity or the sensitivity to Der p 1 and S/T, thus indicating that S/T is an indicator of the releasability of histamine. When basophils or mast cells were passively sensitized with mouse IgE and subsequently stimulated with antimouse IgE, the reactivity to antihuman IgE was significantly correlated with that to antimouse IgE (rs = 0.966, P = 0.0023, n = 11). These observations suggest that an intrinsic cellular property regulates reactivity in immunologic histamine release. Taken together, our results suggest that an intrinsic cellular property, as well as specific IgE antibody levels on the cell surface, is an important factor in determining histamine release in response to IgE-dependent activation.