The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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doi:10.1084/jem.20090246
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
© Nowak et al.
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BRIEF DEFINITIVE REPORT

 IL-9 as a mediator of Th17-driven inflammatory disease

Elizabeth C. Nowak1, Casey T. Weaver2, Henrietta Turner2, Sakhina Begum-Haque1, Burkhard Becher3, Bettina Schreiner3, Anthony J. Coyle4, Lloyd H. Kasper1, and Randolph J. Noelle1

1 Department of Microbiology and Immunology, Dartmouth Medical School and the Norris Cotton Cancer Center, Lebanon, NH 03756
2 Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294
3 Institute of Experimental Immunology, Department of Pathology, University Hospital of Zurich, 8057 Zurich, Switzerland
4 Department of Autoimmunity and Inflammation, MedImmune, Gaithersburg, MD 20878

CORRESPONDENCE Randolph J. Noelle: rjn{at}dartmouth.edu

We report that like other T cells cultured in the presence of transforming growth factor (TGF) β, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-β as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6–producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.

Abbreviations used: CNS, central nervous system; EAE, experimental autoimmune encephalomyelitis; MC, mast cell; MOG, myelin oligodendrocyte peptide; qRT-PCR, quantitative real-time PCR.

© 2009 Nowak et al.
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