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IL-4 Is a Critical Determinant in the Generation of Allergic Inflammation Initiated by a Constitutively Active Stat6

Sarita Sehra^*,, Heather A. Bruns^¶, Ayele-Nati N. Ahyi^*,,, Evelyn T. Nguyen^*,, Nathan W. Schmidt^*,, E. Grace Michels^*, Götz-Ulrich von Bülow and Mark H. Kaplan^1,*,,,

^* Department of Pediatrics and Department of Microbiology and Immunology, Herman B. Wells Center for Pediatric Research and Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202; and ^¶ Department of Biology, Ball State University, Muncie, IN 47306

IL-4 is required for the pathogenesis of atopic diseases and immune regulation. Stat6 is critical for IL-4-induced gene expression and Th cell differentiation. Recently, we have generated mice expressing a mutant Stat6 (Stat6VT) under control of the CD2 locus control region that is transcriptionally active independent of IL-4 stimulation. To determine whether active Stat6 in T cells is sufficient to alter immune regulation in vivo, we mated Stat6VT transgenic mice to IL-4-deficient mice. Stat6VT expression in IL-4-deficient lymphocytes was sufficient to alter lymphocyte homeostasis and promote Th2 differentiation in vitro. HyperTh2 levels in Stat6 transgenic mice correlated with an atopic phenotype that manifested as blepharitis and pulmonary inflammation with a high level of eosinophilic infiltration. In the absence of endogenous IL-4, Stat6VT transgenic mice were protected from allergic inflammation. Thus, in mice with hyperTh2 immune responses in vivo, IL-4 is a critical effector cytokine.

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 Address correspondence and reprint requests to Dr. Mark H. Kaplan, Department of Pediatrics, Herman B. Wells Center for Pediatric Research, 702 Barnhill Drive, RI 2600, Indiana University School of Medicine, Indianapolis, IN 46202. E-mail address: mkaplan2{at}iupui.edu

² Abbreviations used in this paper: IRS, insulin receptor substrate; BAL, bronchoalveolar lavage.