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RI Expression in Mouse Mast Cells1
* Department of Biology, Virginia Commonwealth University, Richmond, VA, 23284;
Department of Biology, University of Richmond, Richmond, VA 23173;
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892
Fc
RI expression and function is a central aspect of allergic disease. Using bone marrow-derived mouse mast cell populations, we have previously shown that the Th2 cytokine IL-4 inhibits FcRI expression and function. In the current study we show that the Th2 cytokine IL-10 has similar regulatory properties, and that it augments the inhibitory effects of IL-4. FcRI down-regulation was functionally significant, as it diminished inflammatory cytokine production and IgE-mediated FcRI up-regulation. IL-10 and IL-4 reduced FcRI 
protein expression without altering the 
or 
subunits. The ability of IL-4 and IL-10 to alter FcRI expression by targeting the -chain, a critical receptor subunit known to modulate receptor expression and signaling, suggests the presence of a Th2 cytokine-mediated homeostatic network that could serve to both initiate and limit mast cell effector function.
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