Monomeric IgE enhances human mast cell chemokine production: IL-4 augments and dexamethasone suppresses the response.

Mouse monoclonal IgE antibodies can promote the survival of mouse bone marrow-derived cultured mast cells and induce the cells to secrete mediators in the absence of known specific antigen. To determine whether human IgE, in the absence of known specific antigen, had effects on the mediator secretion or survival of human mast cells. We tested whether human IgE induced human cord blood-derived mast cells to secrete mediators or enhanced their survival on withdrawal of stem cell factor. Exposure to IgE, but not IgG, at concentrations as low as 2.5 microg/mL significantly enhanced the release of IL-8 and monocyte chemoattractant protein 1, but not histamine or cysteinyl leukotrienes. However, under the conditions tested, chemokine production in response to IgE alone was significantly less than that induced when aliquots of the same IgE-sensitized populations of human mast cells were stimulated with anti-IgE. The production of IL-8 and monocyte chemoattractant protein 1 in response to either IgE alone or IgE and anti-IgE was enhanced by preincubation of the cells in IL-4 and was inhibited by preincubation of the cells with dexamethasone. By contrast, we did not detect any ability of IgE to enhance mast cell survival on withdrawal of stem cell factor. Exposure to human IgE in vitro in the absence of known specific antigen can enhance chemokine production by human mast cells, and this secretory response can be enhanced by preincubation of the mast cells with IL-4 and can be suppressed by dexamethasone.