Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Smeets, Ruben; Loo, Fons A. J. van de; Arntz, Onno J.; Bennink, Miranda B.; Joosten, Leo A. B.; Berg, Wim B. van den

doi:10.1038/sj.gt.3301986

Cited by 88 publications

(49 citation statements)

References 37 publications

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“…Significantly elevated levels of IL-18 are present in the synovial fluid, synovial tissue (ST), and sera of patients with rheumatoid arthritis (RA) compared with patients with osteoarthritis (OA) (4). Studies with murine models of RA show that IL-18 plays a key role in the pathogenesis of arthritis, since the administration of IL-18 to mice with collagen-induced arthritis (CIA) increases the severity of arthritis, and its blockade suppresses joint swelling in the murine streptococcal cell wall-induced arthritis model (5,6) and ameliorates arthritis in murine CIA (4).…”

mentioning

confidence: 99%

Interleukin‐18 induces angiogenic factors in rheumatoid arthritis synovial tissue fibroblasts via distinct signaling pathways

Amin

Mansfield

Pákozdi

et al. 2007

Arthritis & Rheumatism

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Objective. Interleukin-18 (IL-18) is a proinflammatory cytokine implicated in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to examine the role of IL-18 in up-regulating secretion of the angiogenic factors stromal cell-derived factor 1␣ (SDF-1␣)/CXCL12, monocyte chemoattractant protein 1 (MCP-1)/CCL2, and vascular endothelial growth factor (VEGF) in RA synovial tissue (ST) fibroblasts, and the underlying signaling mechanisms involved.Methods. We used enzyme-linked immunosorbent assays, Western blotting, and chemical inhibitors/ antisense oligodeoxynucleotides to signaling intermediates to assess the role of IL-18.Results.

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mentioning

confidence: 99%

Interleukin‐18 induces angiogenic factors in rheumatoid arthritis synovial tissue fibroblasts via distinct signaling pathways

Amin

Mansfield

Pákozdi

et al. 2007

Arthritis & Rheumatism

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“…Only the anti-IL-18 monoclonal antibody, however, had a significant effect on established synovitis. In another animal model, the introduction of the murine IL-18 binding protein C via an adenoviral vector resulted in amelioration of CIA [69]. Further studies are needed in humans to establish its safety and efficacy as a potential treatment in RA.…”

Section: Il-18mentioning

confidence: 97%

Rheumatoid arthritis: developing pharmacological therapies

Abbott

Moreland

2004

Expert Opinion on Investigational Drugs

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Rheumatoid arthritis (RA) is a chronic inflammatory disease that often results in significant morbidity, mortality and disability. Over the past 20 years a better understanding of the pathogenesis of RA has led to the development of new approaches to disease treatment. The recent introduction of biological agents has changed the treatment paradigm for RA. The success of early biological therapies including TNF-alpha and IL-1 antagonists has spurred interest in the development of additional novel targets in the treatment of RA. Biological therapies approved for other indications, such as rituximab, are now being evaluated for the treatment of rheumatic diseases such as RA. A co-stimulatory blocker, abatacept, is also in pivotal Phase III trials. This article reviews evolving pharmacological therapies in RA with an emphasis on the newer approaches to treatment including inhibition of cognate signalling and T- and B-cell targets.

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“…37 Several approaches for targeting IL-18 are in development, including IL-18BP, anti-IL-18 antibody and the inhibition of IL-18 secretion via inhibition of caspase 1or antagonism of the proinflammatory purinergic receptor P2X7. IL-18 represents a general amplification factor for many components of innate and adaptive immune responses and, as such, data on the effects of its inhibition in early clinical trials are eagerly awaited.…”

Section: Il-18 Binding Proteinmentioning

confidence: 99%

Cytokine networks—towards new therapies for rheumatoid arthritis

2005

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Success achieved so far in the blockade of tumor necrosis factor and interleukin (IL)-1 in rheumatoid arthritis exemplifies the feasibility and potential therapeutic application of antagonizing cytokine signaling. Despite these advances, there remains a considerable unmet clinical need in this field. A number of preclinical development programs are ongoing to target a variety of cytokines that are central to immune regulation and tissue-matrix destruction in rheumatoid arthritis. Evidence indicates that IL-6 antagonists might represents a useful approach and preliminary data similarly identify IL-15 as an intriguing target. Numerous additional cytokines are under investigation at the preclinical stage, including IL-12-IL-23, IL-17 and IL-18. As therapeutic goals move from disease control towards remission induction, development of the capacity for cytokine targeting to modify the underlying immune dysregulation remains a major priority.

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Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Cited by 88 publications

References 37 publications

Interleukin‐18 induces angiogenic factors in rheumatoid arthritis synovial tissue fibroblasts via distinct signaling pathways

Interleukin‐18 induces angiogenic factors in rheumatoid arthritis synovial tissue fibroblasts via distinct signaling pathways

Rheumatoid arthritis: developing pharmacological therapies

Cytokine networks—towards new therapies for rheumatoid arthritis

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