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Regulation of inflammatory responses by IL-17F

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 n...

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Autores principales: Yang, Xuexian O., Chang, Seon Hee, Park, Heon, Nurieva, Roza, Shah, Bhavin, Acero, Luis, Wang, Yi-Hong, Schluns, Kimberly S., Broaddus, Russell R., Zhu, Zhou, Dong, Chen
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2373839/
https://www.ncbi.nlm.nih.gov/pubmed/18411338
http://dx.doi.org/10.1084/jem.20071978
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author Yang, Xuexian O.
Chang, Seon Hee
Park, Heon
Nurieva, Roza
Shah, Bhavin
Acero, Luis
Wang, Yi-Hong
Schluns, Kimberly S.
Broaddus, Russell R.
Zhu, Zhou
Dong, Chen
author_facet Yang, Xuexian O.
Chang, Seon Hee
Park, Heon
Nurieva, Roza
Shah, Bhavin
Acero, Luis
Wang, Yi-Hong
Schluns, Kimberly S.
Broaddus, Russell R.
Zhu, Zhou
Dong, Chen
author_sort Yang, Xuexian O.
collection PubMed
description 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.
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spelling pubmed-23738392008-11-12 Regulation of inflammatory responses by IL-17F Yang, Xuexian O. Chang, Seon Hee Park, Heon Nurieva, Roza Shah, Bhavin Acero, Luis Wang, Yi-Hong Schluns, Kimberly S. Broaddus, Russell R. Zhu, Zhou Dong, Chen J Exp Med Articles 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. The Rockefeller University Press 2008-05-12 /pmc/articles/PMC2373839/ /pubmed/18411338 http://dx.doi.org/10.1084/jem.20071978 Text en © 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/).
spellingShingle Articles
Yang, Xuexian O.
Chang, Seon Hee
Park, Heon
Nurieva, Roza
Shah, Bhavin
Acero, Luis
Wang, Yi-Hong
Schluns, Kimberly S.
Broaddus, Russell R.
Zhu, Zhou
Dong, Chen
Regulation of inflammatory responses by IL-17F
title Regulation of inflammatory responses by IL-17F
title_full Regulation of inflammatory responses by IL-17F
title_fullStr Regulation of inflammatory responses by IL-17F
title_full_unstemmed Regulation of inflammatory responses by IL-17F
title_short Regulation of inflammatory responses by IL-17F
title_sort regulation of inflammatory responses by il-17f
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2373839/
https://www.ncbi.nlm.nih.gov/pubmed/18411338
http://dx.doi.org/10.1084/jem.20071978
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