The Journal of Experimental Medicine
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Published online April 14, 2008
doi:10.1084/jem.20071978
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Yang et al.
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ARTICLE

 Regulation of inflammatory responses by IL-17F

Xuexian O. Yang1, Seon Hee Chang1, Heon Park3, Roza Nurieva1, Bhavin Shah1, Luis Acero1, Yi-Hong Wang1, Kimberly S. Schluns1, Russell R. Broaddus2, Zhou Zhu4, and Chen Dong1

1 Department of Immunology and 2 Department of Pathology, M.D. Anderson Cancer Center, Houston, TX 77030
3 Department of Immunology, University of Washington, Seattle, WA 98195
4 Johns Hopkins University, Baltimore, MD 21224

CORRESPONDENCE Chen Dong: cdong{at}mdanderson.org

Although interleukin (IL) 17 has been extensively characterized, the function of IL-17F, which has an expression pattern regulated similarly to IL-17, is poorly understood. We show that like IL-17, IL-17F regulates proinflammatory gene expression in vitro, and this requires IL-17 receptor A, tumor necrosis factor receptor–associated factor 6, and Act1. In vivo, overexpression of IL-17F in lung epithelium led to infiltration of lymphocytes and macrophages and mucus hyperplasia, similar to observations made in IL-17 transgenic mice. To further understand the function of IL-17F, we generated and analyzed mice deficient in IL-17F or IL-17. IL-17, but not IL-17F, was required for the initiation of experimental autoimmune encephalomyelitis. Mice deficient in IL-17F, but not IL-17, had defective airway neutrophilia in response to allergen challenge. Moreover, in an asthma model, although IL-17 deficiency reduced T helper type 2 responses, IL-17F–deficient mice displayed enhanced type 2 cytokine production and eosinophil function. In addition, IL-17F deficiency resulted in reduced colitis caused by dextran sulfate sodium, whereas IL-17 knockout mice developed more severe disease. Our results thus demonstrate that IL-17F is an important regulator of inflammatory responses that seems to function differently than IL-17 in immune responses and diseases.

Abbreviations used: BALF, bronchoalveolar lavage fluid; CC10, Clara cell 10; CNS, central nervous system; DSS, dextran sulfate sodium; EAE, experimental autoimmune encephalomyelitis; FAP, allergenic fungal proteinase; H&E, hematoxylin and eosin; MEF, mouse embryonic fibroblast; MMP, matrix metalloproteinase; MOG, myelin oligodendrocyte glycoprotein; PAS, periodic acid Schiff; TRAF6, TNFR-associated factor 6.

X.O. Yang and S.H. Chang contributed equally to this study.


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