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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2814-2820.
Prepublished online as a Blood First Edition Paper on November 29, 2005; DOI 10.1182/blood-2005-09-3610.
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Submitted September 8, 2005
Accepted November 18, 2005
De novo synthesis of early growth response factor-1 is required for the full responsiveness of mast cells to produce TNF and IL-13 by IgE + antigen stimulation
Bo Li, Melanie R Power, and Tong-Jun Lin*
Department of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada; Department of Pediatrics, Dalhousie University, Halifax, NS, Canada
* Corresponding author; email: tong-jun.lin{at}dal.ca.
Early growth-response factor 1 (Egr-1) is a zinc-finger transcription factor that plays a regulatory role in the expression of many genes important for inflammation. Whether Egr-1 is involved in IgE-dependent mast cell activation was investigated. We demonstrated that IgE + antigen (TNP) stimulation induced a rapid expression of Egr-1 mRNA in mouse bone marrow-derived mast cells (BMMC). As early as 15 - 20 min after IgE + TNP stimulation, Egr-1 protein was detectable in the nucleus of BMMC by immuno-fluorescence or electrophoretic mobility shift assay. To examine a role for Egr-1 in IgE-dependent cytokine production by mast cells, Egr-1 deficient (Egr-1-/-) BMMC were developed from the bone marrow cells of Egr-1 knockout mice. Egr-1-/- BMMC express similar levels of surface c-kit and IgE receptor as compared with those on Egr-1+/+ BMMC. Importantly, IgE + TNP-induced TNF and IL-13 expression was significantly reduced at both mRNA and protein levels in Egr-1-/- BMMC as compared with those in Egr-1+/+ BMMC. Thus, our results suggest that de novo synthesis of Egr-1 represents a novel mechanism in Fc RI signaling and is required for the full responsiveness of IgE-dependent TNF and IL-13 production by mast cells.
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