Reduction of interleukin‐17–induced inhibition of chondrocyte proteoglycan synthesis in intact murine articular cartilage by interleukin‐4

Lubberts, Erik; Joosten, Leo A. B.; Loo, Fons A. J. van de; Bersselaar, L. A. M. Van Den; Berg, Wim B. van den

doi:10.1002/1529-0131(200006)43:6<1300::aid-anr12>3.0.co;2-d

Cited by 97 publications

(63 citation statements)

References 37 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%

“…IL-17 has biologic activities similar to those of IL-1␤, and additive/ synergistic effects with IL-1␤ and TNF␣ have been reported (19). In vitro, IL-17 suppresses matrix synthesis by articular chondrocytes through enhancement of nitric oxide (NO) production (20,21). In addition, in vitro studies suggested a role for IL-17 in bone erosion by induction of receptor activator of NF-B ligand (RANKL) expression (22).…”

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confidence: 99%

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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

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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%

mentioning

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

Self Cite

659

457

View full text Add to dashboard Cite

show abstract

“…IL-17 and IL-1 show many similarities with regard to their actions on cytokine induction and joint pathology. IL-17 has similar effects on chondrocyte metabolism and cartilage degradation, although it seems less potent than IL-1 (10,12). Both cytokines can recruit TRAF6 and activate NF-B and activator protein 1 (4,5), although differences in the effects of these transcription factors have also been described (32).…”

Section: Discussionmentioning

confidence: 99%

Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

Koenders¹,

Lubberts²,

Oppers‐Walgreen³

et al. 2005

Arthritis & Rheumatism

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Objective. To examine the capacity of T cell interleukin-17A (IL-17A; referred to hereinafter as IL-17) to induce cartilage damage during experimental arthritis in the absence of IL-1.Methods. Local IL-17 gene transfer was performed in the knee joint of IL-1-deficient mice and wild-type controls during streptococcal cell wall (SCW)-induced arthritis. Knee joints were isolated at various time points for histologic analysis of cartilage proteoglycan (PG) depletion. Expression of messenger RNA for inducible nitric oxide synthase, matrix metalloproteinases (MMPs) 3, 9, and 13, and ADAMTS-4 was determined by quantitative polymerase chain reaction analysis. VDIPEN staining was analyzed to study MMPmediated cartilage damage. In addition, systemic anti-IL-1␣/␤ antibody treatment was performed in mice immunized with type II collagen and injected locally with an adenoviral vector expressing IL-17 or with control adenovirus. Knee joints were isolated and analyzed for cartilage PG depletion, chondrocyte death, and cartilage surface erosion. Conclusion. These data show the capacity of IL-17 to replace the catabolic function of IL-1 in cartilage damage during experimental arthritis. Results. During SCW-induced arthritis

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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

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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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Reduction of interleukin‐17–induced inhibition of chondrocyte proteoglycan synthesis in intact murine articular cartilage by interleukin‐4

Cited by 97 publications

References 37 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

Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

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

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