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Roy J. and Lucille A. Carver College of Medicine, University of Iowa and Veterans Administration Medical Center, Iowa City, IA 52242
The mechanisms regulating IL-4 mRNA stability in differentiated T cells are not known. We found that early exposure of CD4+ T cells to endogenous IL-4 increased IL-4 mRNA stability. This effect of IL-4 was mediated by the RNA-binding protein HuR. IL-4 mRNA interacted with HuR and the dominant binding site was shown within the coding region of IL-4 mRNA. Exposure of CD4+ T cells to IL-4 had no effects on HuR expression or subcellular localization, but triggered HuR binding to IL-4 mRNA. Thus, IL-4 plays a positive role in maintaining IL-4 mRNA stability in CD4+ T cells via a HuR-mediated mechanism.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by a Veterans Administration Merit Review Grant, Grants HL073967, HL077431, HL007638, and RR00059 from the National Center for Research Resources, National Institutes of Health, and General Clinical Research Centers Program (to G.W.H.).
2 T.O.Y. and N.S.B. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Timur O. Yarovinsky, Division of Pulmonary, Critical Care, and Occupational Medicine, 100 Eckstein Medical Research Building, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242. E-mail address: timur-yarovinsky{at}uiowa.edu
4 Abbreviations used in this paper: TTP, tristetraprolin; ActD, actinomycin D; HPRT, hypoxanthine phosphoribosyltransferase; UTR, untranslated region; KO, knockout; shRNA, short hairpin RNA.
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