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

Elizabeth C. Nowak(Dartmouth College), Casey T. Weaver(University of Alabama at Birmingham), Henrietta Turner(University of Alabama at Birmingham), Sakhina Begum-Haque(Dartmouth College), Burkhard Becher(University Hospital of Zurich), Bettina Schreiner(University Hospital of Zurich), Anthony J. Coyle, Lloyd H. Kasper(Dartmouth College), Randolph J. Noelle(Dartmouth College)
The Journal of Experimental Medicine
July 13, 2009
Cited by 394Open Access
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Abstract

We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta 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.


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