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Regulation of inflammatory responses by IL-17F
Open accessAbstract
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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In the citing paper
“Fate-mapping studies using IL-17-fate reporter mice showed IL-23R-dependent differentiation of IL-17-producing cells into encephalitogenic IFNγ-producing Th1/Th17 cells”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
In the citing paper
“Use of cell fate reporter mice showed that T cells that initially express IL-17 (ex-Th17 cells) can subsequently express proinflammatory cytokines, including IFNγ and GM-CSF [38, 76].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
In the citing paper
“Under inflammatory conditions, tissue Th17 cells have been reported to exhibit plastic changes in their effector programs.”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
In the citing paper
“In the absence of IL-23, Th17 cells lose the ability to up-regulate IFNγ and GM-CSF [76].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
In the citing paper
“A key driver of the Th17 cell transition towards a pathogenic phenotype is the cytokine IL-23.”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
In the citing paper
“This conclusion is further supported by the findings that GM-CSF+ T cells co-express a great variety of other cytokines including IL-2, IL-3, IL-4, IL-6, IL-13, IL-17A, IL-22, IFNγ, and TNF [33, 36, 76, 175].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [76]
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Metadata
- Authors
- Yang, X. O., Chang, S. H., Park, H., Nurieva, R., Shah, B., Acero, L., Wang, Y.-H., Schluns, K. S., Broaddus, R. R., Zhu, Z., & Dong, C.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- 1Department of Immunology
- University of Washington (US)
- Johns Hopkins University (US)
- ORCID
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2008-04-14
- Volume
- 205
- Issue
- 5
- Pages
- 1063-1075
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2373839
- OpenAlex
- W2110264653
- Cited by
- 739
- References
- 47
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 18 · 2023: 27 · 2022: 40 · 2021: 31 · 2020: 33 · 2019: 27 · 2018: 38 · 2017: 45 · 2016: 39 · 2015: 54 · 2014: 56 · 2013: 56 · 2012: 54
- FWCI
- 28.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-17F, IL-17, inflammation, IL-17 receptor A, TRAF6, Act1, pro-inflammatory gene expression, lung epithelium, experimental autoimmune encephalomyelitis, airway neutrophilia, allergen challenge, asthma, Th2 immune response, eosinophils, colitis, dextran sulfate
- MeSH terms
- Animals, Cell Line, Fibroblasts, Homeostasis, Inflammation, Lymphocyte Activation, Mice, Transgenic, T-Lymphocytes, Transfection, CD4-Positive T-Lymphocytes, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Interleukin-17, Mice
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