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Cited by 1,536Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis

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Komiyama, Yutaka, Nakae, Susumu, Matsuki, Taizo, Nambu, Aya, Ishigame, Harumichi, Kakuta, Shigeru, Sudo, Katsuko, Iwakura, Yoichiro·2006·The Journal of Immunology
DOI 10.4049/jimmunol.177.1.566
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Abstract

IL-17 is a proinflammatory cytokine that activates T cells and other immune cells to produce a variety of cytokines, chemokines, and cell adhesion molecules. This cytokine is augmented in the sera and/or tissues of patients with contact dermatitis, asthma, and rheumatoid arthritis. We previously demonstrated that IL-17 is involved in the development of autoimmune arthritis and contact, delayed, and airway hypersensitivity in mice. As the expression of IL-17 is also augmented in multiple sclerosis, we examined the involvement of this cytokine in these diseases using IL-17−/− murine disease models. We found that the development of experimental autoimmune encephalomyelitis (EAE), the rodent model of multiple sclerosis, was significantly suppressed in IL-17−/− mice; these animals exhibited delayed onset, reduced maximum severity scores, ameliorated histological changes, and early recovery. T cell sensitization against myelin oligodendrocyte glycoprotein was reduced in IL-17−/− mice upon sensitization. The major producer of IL-17 upon treatment with myelin digodendrocyte glycopritein was CD4+ T cells rather than CD8+ T cells, and adoptive transfer of IL-17−/− CD4+ T cells inefficiently induced EAE in recipient mice. Notably, IL-17-producing T cells were increased in IFN-γ−/− cells, while IFN-γ-producing cells were increased in IL-17−/− cells, suggesting that IL-17 and IFN-γ mutually regulate IFN-γ and IL-17 production. These observations indicate that IL-17 rather than IFN-γ plays a crucial role in the development of EAE.

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  • Th17 cells are a major contributor to the pathogenicity of several inflammatory and autoimmune conditions.

    “a subset of CD4+ T cells that is a major contributor to the pathogenicity of several inflammatory and autoimmune conditions (9–11)”

    From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [11]

    The Discussion (page unavailable) says IL-17-producing cells play a major role in two autoimmune models, EAE and collagen-induced arthritis, and the Results identify CD4+ T cells as the predominant IL-17 producers during EAE. It does not establish that Th17 cells are major pathogenic contributors across inflammatory and autoimmune conditions generally; the Discussion also identifies conditions that are not IL-17-dependent. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Inflammatory subtypes of T cells, particularly Th17 cells, are deleterious in diseases such as multiple sclerosis.

    “inflammatory subtypes of T cells, particularly Th17 cells, are clearly deleterious in diseases such as multiple sclerosis (9–11, 24)”

    From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [11]

    The Abstract reports that EAE, a rodent model of multiple sclerosis, was markedly suppressed in IL-17-deficient mice and that CD4+ T cells were its major IL-17 producers. It also reports elevated IL-17 in patients with multiple sclerosis, but says its contribution to the human disease is suggested rather than established. The claim's certainty about Th17 cells being deleterious in multiple sclerosis exceeds what this paper shows. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Th17 cells are deleterious to the CNS.

    “Th17 cells are deleterious to the CNS”

    From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [11]

    The Abstract and the section on EAE induction by CD4 T cells (page not available in our copy) show that IL-17-producing CD4 T cells promote a mouse disease marked by CNS inflammation and demyelination. That supports a deleterious role in this EAE model, but the unqualified claim extends beyond the condition the paper studied. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • IL-6 drives the production of Th17 cells.

    “IL-6, which drives the production of T helper 17 (Th17) cells”

    From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [11]

    The section on CD4+ T cells during EAE identifies those cells as the main IL-17 producers, but does not discuss IL-6 driving Th17-cell production. A search for IL-6 and Th17 differentiation found no passage addressing that relationship; the paper instead reports that IL-23 promoted IL-17 production. Page numbers were not available in our copy. (LLM, conf=0.74)

    Experimental — accuracy not yet measured

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Cites

Flagged first, then by citations

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Authors
Komiyama, Y., Nakae, S., Matsuki, T., Nambu, A., Ishigame, H., Kakuta, S., Sudo, K., & Iwakura, Y.
Affiliations
Institute of Medical Science, The University of Tokyo (JP)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2006-07-01
Volume
177
Issue
1
Pages
566-573
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.177.1.566
OpenAlex
W1959664751
Cited by
1,536
References
54
Citations by year
2026: 12 · 2025: 18 · 2024: 30 · 2023: 30 · 2022: 56 · 2021: 47 · 2020: 44 · 2019: 53 · 2018: 70 · 2017: 72 · 2016: 62 · 2015: 80 · 2014: 97 · 2013: 102 · 2012: 120
FWCI
89.46
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
School of Medicine, Stanford University
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
IL-17, experimental autoimmune encephalomyelitis, multiple sclerosis, interferon-gamma, myelin oligodendrocyte glycoprotein, CD4+ T cells, T cell sensitization, adoptive transfer, cytokine regulation, autoimmune disease
MeSH terms
Amino Acid Sequence, Animals, Autoantibodies, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Glycoproteins, Interferon-gamma, Lymph Nodes, Mice, Inbred C57BL, Molecular Sequence Data, Peptide Fragments, CD4-Positive T-Lymphocytes, Up-Regulation, Mice, Knockout, Epitopes, T-Lymphocyte, Adoptive Transfer, Interleukin-17, Mice, Myelin-Oligodendrocyte Glycoprotein

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