IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?

Lubberts, Erik

doi:10.1016/j.cyto.2007.09.014

Cited by 289Rheumatoid Arthritis Research and TherapiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?

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Lubberts, Erik·2008·Cytokine

DOI 10.1016/j.cyto.2007.09.014

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Abstract

Interleukin-17A (IL-17A) contributes to the pathogenesis of arthritis. Data from experimental arthritis indicate IL-17 receptor signaling as a critical pathway in turning an acute synovitis into a chronic destructive arthritis. The identification of six IL-17 family members (IL-17A-F) may extend the role of this novel cytokine family in the pathogenesis of chronic destructive joint inflammation. Whether the successful anti-IL-17A cytokine therapy in murine arthritis can be effectively translated to human arthritis need to be tested in clinical trials in humans. Interestingly, IL-17A and IL-17F are secreted by the novel T helper subset named Th17. This novel pathogenic T cell population induces autoimmune inflammation in mice and is far more efficient at inducing Th1-mediated autoimmune inflammation in mice than classical Th1 cells (IFN-gamma). In addition to IL-17A and IL-17F, Th17 cells are characterized by expression of IL-6, TNF, GM-CSF, IL-21, IL-22 and IL-26. Th17 cells have been established as a separate lineage of T helper cells in mice distinct from conventional Th1 and Th2 cells. Whether this also applies to human Th17 and whether RA is a Th1 or a Th17 mediated disease is still not clear. This review summarizes the findings about the role of IL-17 in arthritis and discusses the impact of the discovery of the novel Th17 cells for arthritis. Further studies are needed to unravel the role of Th17 cells and the interplay of IL-17 and other Th17 cytokines in the pathogenesis of arthritis and whether regulating Th17 cell activity will have additional value compared to neutralizing IL-17A activity alone. This might help to reach the ultimate goal not only to treat RA patients but to prevent the development of this crippling disease.

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Multiple studies have highlighted a critical role of the intestinal microbiota in the development of extra-intestinal autoimmune diseases.
“Multiple studies have highlighted a critical role of the intestinal microbiota in the development of extra-intestinal autoimmune diseases [88, 184–186].”
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Authors: Lubberts, E.
Affiliations: Erasmus MC (NL)
Corresponding author: Lubberts, Erik
ORCID: Lubberts, Erik
Venue: Cytokine
Publisher: Elsevier BV
Published: 2008-02
Volume: 41
Issue: 2
Pages: 84-91
ISSN: 1043-4666 (ISSN-L)
DOI: 10.1016/j.cyto.2007.09.014
OpenAlex: W2001857046
Cited by: 289
References: 78
Citations by year: 2026: 3 · 2025: 3 · 2024: 6 · 2023: 10 · 2022: 7 · 2021: 8 · 2020: 9 · 2019: 12 · 2018: 8 · 2017: 16 · 2016: 16 · 2015: 19 · 2014: 21 · 2013: 10 · 2012: 26
FWCI: 3.82
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cytokine (publishedVersion)
PubMed (publishedVersion)
EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, other-oa)
EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
RePub (Erasmus University Rotterdam) (submittedVersion)
Topics: Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: IL-17A, IL-17F, Th17 cells, rheumatoid arthritis, IL-17 receptor signaling, synovitis, Th1-mediated inflammation, IL-17 family cytokines, anti-IL-17A therapy, arthritis prevention, T helper cell differentiation
MeSH terms: Animals, Arthritis, Rheumatoid, T-Lymphocytes, Helper-Inducer, Humans, Interleukin-17, Receptors, Interleukin-17

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IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?

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