Abstract
The cytokine interleukin (IL)-3 is important in the proliferation of eosinophils and basophils in the airway. We investigated IL-3 production by human lung mast cells as a possible mechanism of the airway inflammation constituting the late asthmatic response. Mast cells were purified using affinity magnetic selection with the monoclonal antibody YB5.B8 and then stimulated with anti-human IgE antibody. IL-3 release was detectable by enzyme-linked immunosorbent assay 8 h after anti-IgE stimulation. IL-3 release 24 h after anti-IgE stimulation was significantly greater than its controls. By reverse transcription-polymerase chain reaction, IL-3 mRNA was detected weakly 2 h after anti-IgE stimulation, peaking at 4 h and waning at 8 h. Immunocytochemistry to localize IL-3 demonstrated mast cell staining. These results suggest that mast cells release IL-3 in response to high-affinity IgE receptor.
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