ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Development of proteoglycan-induced arthritis is independent of IL-17.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 98 citations in OpenAlex.
- The dual role of IL-17 in periodontitis regulating immunity and bone homeostasis.Frontiers in immunology · 2025Review
- Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective.The Journal of experimental medicine · 2020Review
- Why Don't We Have a Vaccine Against Autoimmune Diseases? - A Review.Journal of clinical & cellular immunology · 2019Article
- STAT6 and IL-10 are required for the anti-arthritic effects of Schistosoma mansoni via different mechanisms.Clinical and experimental immunology · 2019Article
- Interleukin-17A is involved in mechanical hyperalgesia but not in the severity of murine antigen-induced arthritis.Scientific reports · 2017Article
- Article
- Arthritis models: usefulness and interpretation.Seminars in immunopathology · 2017Review
- Modulation of PBMC-decay accelerating factor (PBMC-DAF) and cytokines in rheumatoid arthritis.Molecular and cellular biochemistry · 2016Article
- Gut Microbiota Regulates K/BxN Autoimmune Arthritis through Follicular Helper T but Not Th17 Cells.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Enigma of IL-17 and Th17 Cells in Rheumatoid Arthritis and in Autoimmune Animal Models of Arthritis.Mediators of inflammation · 2016Review
- The IL-23-IL-17 axis in inflammatory arthritis.Nature reviews. Rheumatology · 2015Review
- T helper subsets in allergic eye disease.Current opinion in allergy and clinical immunology · 2014Review
- Tissue specific CD4+ T cell priming determines the requirement for interleukin-23 in experimental arthritis.Arthritis research & therapy · 2014Article
- Of mice and men: how animal models advance our understanding of T-cell function in RA.Nature reviews. Rheumatology · 2014Review
- Brief report: Autologous stem cell transplantation restores immune tolerance in experimental arthritis by renewal and modulation of the Teff cell compartment.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Proteoglycan aggrecan conducting T cell activation and apoptosis in a murine model of rheumatoid arthritis.BioMed research international · 2014Review
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- Location of CD4+ T cell priming regulates the differentiation of Th1 and Th17 cells and their contribution to arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- The choice of adjuvant determines the cytokine profile of T cells in proteoglycan-induced arthritis but does not influence disease severity.Immunology · 2013Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
IL-17 is the hallmark cytokine for the newly identified subset of Th cells, Th17. Th17 cells are important instigators of inflammation in several models of autoimmune disease; in particular, collagen induced arthritis (CIA) and experimental autoimmune encephalomyelitis (EAE), which were previously characterized as Th1-mediated diseases. Although high levels of IFN-gamma are secreted in CIA and EAE, disease is exacerbated in IFN-gamma- or IFN-gamma receptor-deficient mice due to the ability of IFN-gamma to suppress IL-17 secretion. However, in proteoglycan-induced arthritis (PGIA), severe arthritis is dependent on the production of IFN-gamma. We were therefore interested in determining the role of IL-17 in PGIA. We assessed the progression of arthritis in IL-17-deficient (IL-17-/-) mice and found the onset and severity of arthritis were equivalent in wild-type (WT) and IL-17-/- mice. Despite evidence that IL-17 is involved in neutrophil recruitment, synovial fluid from arthritic joints showed a comparable proportion of Gr1+ neutrophils in WT and IL-17-/- mice. IL-17 is also implicated in bone destruction in autoimmune arthritis, however, histological analysis of the arthritic joints from WT and IL-17-/- mice revealed a similar extent of joint cellularity, cartilage destruction, and bone erosion despite significantly reduced RANKL (receptor activator of NK-kappaB ligand) expression. There were only subtle differences between WT and IL-17-/- mice in proinflammatory cytokine expression, T cell proliferation, and autoantibody production. These data demonstrate that IL-17 is not absolutely required for autoimmune arthritis and that the production of other proinflammatory mediators is sufficient to compensate for the loss of IL-17 in PGIA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.