Mast cells play an important role in initiating and modulating allergic and inflammatory reactions. Their responsiveness is determined by three important factors: the expression of IgE receptors on the cell surface, the IgE occupancy of these receptors, and the intrinsic secretory capacity of the cells. In this review, we will summarise some findings relevant to these three aspects of mast cell function, and discuss possible regulatory mechanisms. It appears that the genetic background as well as environmental factors influence all three of these components of the response. T cells appear to play an important role in regulating the IgE-receptor expression and also, independently, the intrinsic secretory capacity of mast cells via an unidentified route, possibly involving the secretory signal transduction chain directly. IgE itself appears to have an important role in the regulation of IgE-receptor expression, as indicated by the upregulation of receptors in vitro in the presence of IgE, and the absence of IgE-binding capacity of mast cells in IL-4 gene knockout mice, lacking IgE production. The IgE-receptors of mast cells are saturated to a high degree under different normal conditions, without an obvious relation to antigenic stimulation, also in athymic animals. We have suggested that this basal IgE content on mast cells may be the result of an antigen-independent production of IgE directed by the mast cells themselves and serving regulatory purposes, modifying the secretory response and preventing a massive possibly harmful degranulation.

In previous works using cytofluorometry, we demonstrated a broad range of IgE and IgE‐receptor levels within individual mast cell populations with a 60 to 80% occupancy of the IgE receptors on mast cells by native IgE. This study was performed in order to confirm our previous findings using an independent method and to visualize the distribution of IgE‐receptor complexes on mast cells at an ultrastructural level. For this purpose an indirect immunocolloidal gold‐labelling technique has been applied. By counting the number of labelled gold particles, a relative measure of IgE‐receptor surface expression and IgE occupancy of the receptors could be obtained. With respect to mast cell morphology and anti‐IgE binding specificity criteria, 1% glutaraldehyde+4% paraformaldehyde (1 : 1, vol/vol) was found to be the best of the seven fixatives applied in this study. This technique revealed numerous gold particles on the surface of mast cells from barrier‐maintained rats (26±11 per mast cell section, mean±SD). Increased numbers of gold particles were counted if the mast cells were incubated with rat myeloma IgE (20 μg/ml) (46±33 per mast cell section, mean±SD). There were significantly increased numbers of gold particles on the mast cells of rats infected with N. brasiliensis (126±30 per mast cell section, mean±SD). This indicates that some of the IgE receptors (about 50% of the total number of IgE receptors in this case) on mast cells were occupied by native IgE and that parasite infection significantly increased the number of IgE molecules on the surface of the mast cells. These results correspond with the findings we have made using the cytofluorometric technique and confirm the large individual variations in the density of IgE receptors and IgE among the mast cells of a given cell population. Macrophages, lymphocytes and eosinophils, carrying the low‐affinity IgE receptors (FcεRII), contained less than 5 (normal rats after incubation in rat IgE) or 10 (nematode‐infected rats) gold particles per cell section. We also observed some non‐granulated lymphocyte‐like cells which bound a large number of gold particles after incubation with rat myeloma IgE (20 μg/ml), indicating that they contained IgE receptors (FcεRI). They were interpreted as mast cell precursors which have previously been shown to exist in the peritoneal cavity.