Effect of interleukin 17 on proteoglycan degradation in murine knee joints

Dudler, Jean

doi:10.1136/ard.59.7.529

Cited by 74 publications

(41 citation statements)

References 22 publications

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“…In vitro, it inhibits chondrocyte metabolism in intact articular cartilage of mice and results in proteoglycan breakdown (19,20,30,31). Furthermore, in vitro studies show the induction of metalloproteinases by IL-17 in synoviocytes and chondrocytes (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Lubberts¹,

Koenders²,

Oppers‐Walgreen³

et al. 2004

Arthritis & Rheumatism

659

457

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Objective. Interleukin-17 (IL-17) is a proinflammatory cytokine that is expressed in the synovium of rheumatoid arthritis (RA) patients. This T cell cytokine is implicated in the initiation phase of arthritis. However, the role of IL-17 during the effector phase of arthritis has still not been identified; this was the objective of the present study.Methods. Mice with collagen-induced arthritis (CIA) were treated with polyclonal rabbit anti-murine IL-17 (anti-IL-17) antibody-positive serum or normal rabbit serum after the first signs of arthritis. In addition, during a later stage of CIA mice were selected and treated with anti-IL-17 antibody or control serum. Arthritis was monitored visually, and joint pathology was examined radiologically and histologically. Systemic IL-6 levels were measured by enzyme-linked immunosorbent assay, and local synovial IL-1 and receptor activator of NF-B ligand (RANKL) expression was analyzed using specific immunohistochemistry.Results

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Section: Discussionmentioning

confidence: 99%

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Lubberts¹,

Koenders²,

Oppers‐Walgreen³

et al. 2004

Arthritis & Rheumatism

659

457

View full text Add to dashboard Cite

show abstract

“…IL-17 was also shown to decrease the synthesis of chondrocyte proteoglycan as well as to increase the loss of proteoglycans from mouse cartilage (28,29). Local IL-17 expression in mouse knee joints resulted in a rapid depletion of proteoglycans (8,30). Moreover, synergistic effects of IL-17 in combination with other proinflammatory cytokines in inducing cartilage damage have been shown in vitro (31,32).…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐17 receptor deficiency results in impaired synovial expression of interleukin‐1 and matrix metalloproteinases 3, 9, and 13 and prevents cartilage destruction during chronic reactivated streptococcal cell wall–induced arthritis

Koenders¹,

Kolls²,

Oppers‐Walgreen³

et al. 2005

Arthritis & Rheumatism

174

134

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Objective. To examine the role of interleukin-17 receptor (IL-17R) signaling in cartilage destruction and its interrelationship with synovial IL-1 expression during chronic reactivated streptococcal cell wall (SCW)-induced arthritis. Methods. SCW arthritis was repeatedly induced in wild-type (WT) and IL-17R-deficient (IL-17R-/-) mice. At different time points, joint inflammation was assessed by using calipers to measure joint swelling. On day 42, mice were killed, and knee joints were removed for histologic analysis. Quantitative polymerase chain reaction (PCR) analyses for different proinflammatory mediators and matrix metalloproteinases (MMPs) were performed on inflamed synovium from WT and IL-17R -/-mice after 5 repeated injections of SCW fragments. Results. IL-17R

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“…In addition to joint inflammation, IL-17 has clear catabolic effects on cartilage and bone [25][26][27][28]29,30]. Studies in IL-17 receptor knockout mice revealed a critical role of IL-17 receptor signaling in driving synovial expression of proinflammatory and catabolic mediators, such as IL-1 and different MMPs leading to less cartilage damage and bone erosion in experimental arthritis [11,31].…”

Section: Experimental Arthritis Studiesmentioning

confidence: 99%

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

Lubberts¹

2008

Cytokine

274

230

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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-c). 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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Effect of interleukin 17 on proteoglycan degradation in murine knee joints

Cited by 74 publications

References 22 publications

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Treatment with a neutralizing anti‐murine interleukin‐17 antibody after the onset of collagen‐induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion

Interleukin‐17 receptor deficiency results in impaired synovial expression of interleukin‐1 and matrix metalloproteinases 3, 9, and 13 and prevents cartilage destruction during chronic reactivated streptococcal cell wall–induced arthritis

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

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