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

被引:314
作者
Nowak, Elizabeth C. [1 ,2 ]
Weaver, Casey T. [3 ]
Turner, Henrietta [3 ]
Begum-Haque, Sakhina [1 ,2 ]
Becher, Burkhard [4 ]
Schreiner, Bettina [4 ]
Coyle, Anthony J. [5 ]
Kasper, Lloyd H. [1 ,2 ]
Noelle, Randolph J. [1 ,2 ]
机构
[1] Dartmouth Med Sch, Dept Microbiol & Immunol, Lebanon, NH 03756 USA
[2] Norris Cotton Canc Ctr, Lebanon, NH 03756 USA
[3] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA
[4] Univ Zurich Hosp, Dept Pathol, Inst Expt Immunol, CH-8057 Zurich, Switzerland
[5] Medimmune Inc, Dept Autoimmun & Inflammat, Gaithersburg, MD 20878 USA
基金
美国国家卫生研究院;
关键词
EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MAST-CELLS; T-CELLS; MURINE MODEL; TGF-BETA; RECEPTOR; DIFFERENTIATION; INTERLEUKIN-9; PROMOTES; CNS;
D O I
10.1084/jem.20090246
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:1653 / 1660
页数:8
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