INFLUENCE OF GENETIC AND ENVIRONMENTAL-FACTORS ON SURFACE EXPRESSION AND OCCUPANCY OF IGE RECEPTORS AND ON HISTAMINE RELEASABILITY OF MAST-CELLS

The relationship between the IgE load on mast cells and their secretory capacity when challenged with anti-IgE was studied in peritoneal cells obtained from rats of three different strains, Hooded Lister (HL), Wistar Kyoto (WKY) and Sprague-Dawley (SD). IgE was determined cytofluorometrically after labelling with FITC-conjugated anti-IgE before and after the saturation of the IgE receptors to provide a measure of the surface expression of IgE receptors (number of receptors available for bindings) as well as the IgE occupancy of the receptors (native IgE content). The secretory capacity of the mast cells was examined in vitro in terms of histamine release as a function of anti-IgE concentration. Mast cells obtained from HL and WKY rats were found to carry significantly higher levels of IgE receptors and IgE than the mast cells of SD rats bred and raised under the same conventional laboratory conditions. The mast cells of SD rats kept under barrier-maintained conditions carried significantly less IgE than the mast cells obtained from SD rats kept under conventional conditions, but their IgE receptor levels were similar. The IgE-mediated histamine-releasing capacity of the mast cells, evaluated in terms of maximum release or of the slopes of regression lines (histamine release versus anti-IgE concentration), was positively correlated to the levels of native IgE and IgE receptors in the three strains of rat combined. The mast cells obtained from WKY rats showed the highest secretory capacity in the three strains of rat examined, significantly higher than the mast cells of HL rats, even though the latter displayed similar levels of IgE and IgE receptors. These findings indicate that under basal conditions in these strains of rat the number of IgE receptors available for binding as well as the IgE occupancy is determined by both the genetic background and the environment. The IgE-mediated histamine release appeared to be largely, but not exclusively a function of the number of IgE-receptor complexes on the mast-cell surface. The difference in histamine-releasing capacity between WKY and HL rats suggests that genetic factors may control the secretory capacity of the mast cells also through mechanisms other than those involving the expression of IgE receptors and the binding of IgE by the mast cells.