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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

FcepsilonRI-dependent gene expression in human mast cells is differentially controlled by T helper type 2 cytokines.

BACKGROUND: Mast cells (MCs) proliferate in response to T(H)2 cytokines and express genes de novo after activation. Limited information is available concerning the interplay between these events. OBJECTIVE: We explored the potential for T(H)2 cytokines to alter activation-dependent gene expression by MCs. METHODS: Cord blood-derived human (h)MCs maintained in stem cell factor ( SCF) alone were compared with replicates treated with IL-4, IL-5, or IL-9, respectively, for their patterns of FcepsilonRI-dependent gene induction using microarray technology. RESULTS: Activation of SCF-treated hMCs upregulated their expression of roughly 140 transcripts at 2 hours, including genes involved in cell cycle progression and arrest. Each cytokine substantially modified this profile; approximately 800 inducible genes apiece were controlled by IL-5 or IL-9, whereas 169 inducible genes were controlled by IL-4. IL-4 favored the induction of cytokines and of genes associated with cell growth arrest (GADD34, GAS-1, CIDE-A, INK4D, and BAX) and completely abolished the enhanced proliferation observed in the other 3 groups after activation. Conversely, IL-5 priming induced preferential upregulation of genes involved in cell proliferation and did not abolish thymidine incorporation. CONCLUSIONS: T(H)2 cytokines differentially modulate gene induction in hMCs after FcepsilonRI cross-linkage. IL-4 uniquely controls cytokine gene expression by hMCs and might also limit their activation-driven proliferation.[1]


  1. FcepsilonRI-dependent gene expression in human mast cells is differentially controlled by T helper type 2 cytokines. Lora, J.M., Al-Garawi, A., Pickard, M.D., Price, K.S., Bagga, S., Sicoli, J., Hodge, M.R., Gutiérrez-Ramos, J.C., Briskin, M.J., Boyce, J.A. J. Allergy Clin. Immunol. (2003) [Pubmed]
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