The role of TRB3 in mast cells sensitized with monomeric IgE.

Authors:
Kei Morohoshi, MD, PhD
Kei Morohoshi, MD, PhD
Emory University School of Medicine
United States

Exp Mol Pathol 2012 Dec 21;93(3):408-15. Epub 2012 Sep 21.

Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, OH 45221-0097, USA.

Mast cells play a key role in immunoglobulin E (IgE)-associated allergic disorders; however, the cellular effects of sensitization remain poorly understood. Using gene microarrays and the multiplexing ELISA method, we examined the effects of sensitization on RBL-CCR1 cell transcription and chemokine/cytokine secretion. Sensitization most prominently increased transcription of Trb3, the gene for tribbles homolog 3 (TRB3), and also increased the release of most of the cytokines and chemokines tested. Knockdown of TRB3 via RNAi significantly induced the production of tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), interleukin-6 (IL-6), and the chemokine mast cell protease-1 (MCP-1). TRB3 deficiency also induced IκBα phosphorylation. TRB3 may therefore serve as a negative regulator of pro-inflammatory cytokines and chemokines, controlling the extent of the inflammatory response.

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http://dx.doi.org/10.1016/j.yexmp.2012.09.008DOI Listing
December 2012
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3 Citations
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