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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...
Autores principales: | , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2008
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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. |
format | Text |
id | pubmed-2373839 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
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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