Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 4608K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yang, X. O. Articles by Dong, C. Search for Related Content PubMed PubMed Citation Articles by Yang, X. O. Articles by Dong, C. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH Social Bookmarking                            What's this?

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.

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

© 2008 Yang et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Smith, E., von Vietinghoff, S., Stark, M. A., Zarbock, A., Sanders, J. M., Duley, A., Rivera-Nieves, J., Bender, T. P., Ley, K. (2009). T-Lineage Cells Require the Thymus but Not V(D)J Recombination to Produce IL-17A and Regulate Granulopoiesis In Vivo. J. Immunol. 183: 5685-5693 [Abstract] [Full Text]  
• Wilson, R. H., Whitehead, G. S., Nakano, H., Free, M. E., Kolls, J. K., Cook, D. N. (2009). Allergic Sensitization through the Airway Primes Th17-dependent Neutrophilia and Airway Hyperresponsiveness. Am. J. Respir. Crit. Care Med. 180: 720-730 [Abstract] [Full Text]  
• von Vietinghoff, S., Ley, K. (2009). IL-17A Controls IL-17F Production and Maintains Blood Neutrophil Counts in Mice. J. Immunol. 183: 865-873 [Abstract] [Full Text]  
• Bordon, Y., Hansell, C. A. H., Sester, D. P., Clarke, M., Mowat, A. McI., Nibbs, R. J. B. (2009). The Atypical Chemokine Receptor D6 Contributes to the Development of Experimental Colitis. J. Immunol. 182: 5032-5040 [Abstract] [Full Text]  
• Zhang, X., Jin, J., Tang, Y., Speer, D., Sujkowska, D., Markovic-Plese, S. (2009). IFN-{beta}1a Inhibits the Secretion of Th17-Polarizing Cytokines in Human Dendritic Cells via TLR7 Up-Regulation. J. Immunol. 182: 3928-3936 [Abstract] [Full Text]  
• Swaidani, S., Bulek, K., Kang, Z., Liu, C., Lu, Y., Yin, W., Aronica, M., Li, X. (2009). The Critical Role of Epithelial-Derived Act1 in IL-17- and IL-25-Mediated Pulmonary Inflammation. J. Immunol. 182: 1631-1640 [Abstract] [Full Text]  
• Hartupee, J., Liu, C., Novotny, M., Sun, D., Li, X., Hamilton, T. A. (2009). IL-17 Signaling for mRNA Stabilization Does Not Require TNF Receptor-Associated Factor 6. J. Immunol. 182: 1660-1666 [Abstract] [Full Text]  
• Kappel, L. W., Goldberg, G. L., King, C. G., Suh, D. Y., Smith, O. M., Ligh, C., Holland, A. M., Grubin, J., Mark, N. M., Liu, C., Iwakura, Y., Heller, G., van den Brink, M. R. M. (2009). IL-17 contributes to CD4-mediated graft-versus-host disease. Blood 113: 945-952 [Abstract] [Full Text]  
• Wakashin, H., Hirose, K., Maezawa, Y., Kagami, S.-i., Suto, A., Watanabe, N., Saito, Y., Hatano, M., Tokuhisa, T., Iwakura, Y., Puccetti, P., Iwamoto, I., Nakajima, H. (2008). IL-23 and Th17 Cells Enhance Th2-Cell-mediated Eosinophilic Airway Inflammation in Mice. Am. J. Respir. Crit. Care Med. 178: 1023-1032 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS