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1 Inhibits Mast Cell Fc
RI Expression 1
* Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Biology Department, University of Richmond, Richmond, VA 23173; and Departments of
Internal Medicine and
Biology, Virginia Commonwealth University, Richmond, VA 23284
Mast cell activation through the high affinity IgE receptor (Fc
RI) is a critical component of atopic inflammation. The cytokine TGF-
1 has been shown to inhibit IgE-dependent mast cell activation, possibly serving to dampen mast cell-mediated inflammatory responses. We present proof that TGF-1 inhibits mast cell FcRI expression through a reversible pathway that diminishes protein, but not mRNA, expression of the FcRI subunit proteins 
, , and 
. The stability of the expressed proteins and the assembled cell surface complex was unaltered by TGF-1 treatment. However, TGF-1 decreased the rate of FcRI -chain synthesis, arguing that this inhibitory cytokine exerts its effects at the level of mRNA translation. TGF-1 consistently diminished FcRI expression on cultured human or mouse mast cells as well as freshly isolated peritoneal mast cells. The related cytokines, TGF-2 and TGF-3, had similar effects. We propose that TGF-1 acts as a negative regulator of mast cell function, in part by decreasing FcRI expression.
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