Cited by 739Psoriasis: Treatment and PathogenesisCytokine Signaling Pathways and InteractionsT-cell and B-cell Immunology

Regulation of inflammatory responses by IL-17F

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Yang, Xuexian O., Chang, Seon Hee, Park, Heon, Nurieva, Roza, Shah, Bhavin, Acero, Luis, Wang, Yi-Hong, Schluns, Kimberly S. +3 more·2008·The Journal of Experimental Medicine

Abstract

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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Crossref · 10.1084/jem.20071978

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  • Fate-mapping studies show IL-23R-dependent differentiation of IL-17-producing cells into encephalitogenic IFNγ-producing Th1/Th17 cells.

    “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]

  • Cell fate reporter mice showed that T cells initially expressing IL-17 (ex-Th17 cells) can subsequently express proinflammatory cytokines including IFNγ and GM-CSF.

    “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]

  • Under inflammatory conditions, tissue Th17 cells exhibit plastic changes in their effector programs.

    “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 absence of IL-23, Th17 cells lose the ability to up-regulate IFNγ and GM-CSF.

    “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]

  • IL-23 is a key driver of the Th17 cell transition towards a pathogenic phenotype.

    “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]

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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)
Venue
The Journal of Experimental Medicine
Published
2008-04-14
Volume
205
Issue
5
Pages
1063-1075
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
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
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
  • Health Sciences › Medicine › Oncology › 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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