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The Journal of Immunology, 1998, 161: 6915-6923.
Copyright © 1998 by The American Association of Immunologists

IL-4 Inhibits Mouse Mast Cell Fc{epsilon}RI Expression Through a STAT6-Dependent Mechanism1

John J. Ryan2,*, Shirley DeSimone{dagger}, Gregory Klisch{dagger}, Christopher Shelburne*, Lisa J. McReynolds*, Kathy Han*, Reka Kovacs*, Paria Mirmonsef* and Thomas F. Huff{dagger}

Departments of * Biology and {dagger} Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23284

Mast cell activation by IgE-mediated stimuli is a central event in atopic disease. The regulation of the mast cell high affinity receptor, Fc{epsilon}RI, is poorly understood. We show that IL-4 can inhibit Fc{epsilon}RI expression on mouse bone marrow-derived mast cells and fetal liver-derived mast cell progenitors. This effect could be observed at 2.5 ng/ml IL-4 and was dose dependent. IL-4-mediated inhibition of cultured BMMC required 4 days of stimulation and was sustained at maximum levels for at least 21 days. The inhibition of Fc{epsilon}RI expression resulted in decreased sensitivity to IgE-mediated stimulation, as measured by serotonin release, and the induction of mRNA for IL-4, IL-5, IL-6, and IL-13. Additionally, IL-4 could abrogate the IgE-mediated increase in Fc{epsilon}RI expression. Lastly, IL-4-mediated inhibition was dependent upon expression of the STAT6 transcription factor, as STAT6-deficient bone marrow-derived mast cells did not decrease Fc{epsilon}RI levels in response to IL-4. These data argue for a homeostatic role of IL-4 in the regulation of Fc{epsilon}RI expression, a role that could be critical to understanding atopic disease.




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