We are analyzing https://link.springer.com/article/10.1186/ar1478.

Title:
The role of T cell interleukin-17 in conducting destructive arthritis: lessons from animal models | Arthritis Research & Therapy
Description:
Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and a strong correlation between IL-15 and IL-17 levels in synovial fluid has been observed. IL-17 is a potent inducer of various cytokines such as tumor necrosis factor (TNF)-α, IL-1, and receptor activator of NF-κB ligand (RANKL). Additive or even synergistic effects with IL-1 and TNF-α in inducing cytokine expression and joint damage have been shown in vitro and in vivo. This review describes the role of IL-17 in the pathogenesis of destructive arthritis with a major focus on studies in vivo in arthritis models. From these studies in vivo it can be concluded that IL-17 becomes significant when T cells are a major element of the arthritis process. Moreover, IL-17 has the capacity to induce joint destruction in an IL-1-independent manner and can bypass TNF-dependent arthritis. Anti-IL-17 cytokine therapy is of interest as an additional new anti-rheumatic strategy for RA, in particular in situations in which elevated IL-17 might attenuate the response to anti-TNF/anti-IL-1 therapy.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, arthritis, google, scholar, cas, article, cells, interleukin, cytokine, mice, cell, cartilage, expression, role, van, inflammation, synovial, production, receptor, joint, immunol, factor, destruction, human, bone, central, lubberts, family, cia, berg, vitro, protein, cytokines, tnfα, rankl, rheum, rheumatoid, activated, function, erosion, produced, inflammatory, members, effects, immune, tnf, activation, synovium, data, levels,

Topics {✒️}

c-jun n-terminal kinase pro-matrix metalloproteinase [pro-mmp]-3 mitogen-activated protein kinase t-cell-derived cytokine t-cell-triggered inflammation lipopolysaccharide-induced airway neutrophilia nf-κb-inducing kinase human skin-derived nickel-specific van der wee-pals fewer il-1β-positive cells murine collagen-induced arthritis coenen-de roo cj coenen-de roo cjj mitogen-activated protein kinases anti-tnf/anti-il-1 therapy unabated il-17-induced exaggeration cii-immunized dba-1 mice delayed-type hypersensitivity responses αβ tcr+cd4-cd8 gene therapy-derived method cii-immunized mice resulted oliveira-dos-santos aj bypass tnf-dependent arthritis adapter molecule tnf-receptor activating autoantigen-specific cellular cyclosporin a-sensitive mechanism attenuates inflammatory arthritis interleukin-17-induced gene expression open-reading frame cytokine receptor-ligand pair cell il-17/il-17r signaling tnf-α-induced synthesis related subjects il-1β-deficient mice [41] human pbmc-derived macrophages van den berg anti-cii immune complexes il-17-induced cytokine release tnf-α-dependent arthritis elastase-mediated proteolytic activity tumor necrosis factor il-17-deficient mice revealed pro-inflammatory cytokine produced type ii collagen il-17-induced synovial inflammation cell-derived cytokine produced il-17-induced joint inflammation cells expressing tnf-α il-17r-deficient mice anti-il-17 cytokine therapy

Schema {🗺️}

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         description:Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and a strong correlation between IL-15 and IL-17 levels in synovial fluid has been observed. IL-17 is a potent inducer of various cytokines such as tumor necrosis factor (TNF)-α, IL-1, and receptor activator of NF-κB ligand (RANKL). Additive or even synergistic effects with IL-1 and TNF-α in inducing cytokine expression and joint damage have been shown in vitro and in vivo. This review describes the role of IL-17 in the pathogenesis of destructive arthritis with a major focus on studies in vivo in arthritis models. From these studies in vivo it can be concluded that IL-17 becomes significant when T cells are a major element of the arthritis process. Moreover, IL-17 has the capacity to induce joint destruction in an IL-1-independent manner and can bypass TNF-dependent arthritis. Anti-IL-17 cytokine therapy is of interest as an additional new anti-rheumatic strategy for RA, in particular in situations in which elevated IL-17 might attenuate the response to anti-TNF/anti-IL-1 therapy.
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      headline:The role of T cell interleukin-17 in conducting destructive arthritis: lessons from animal models
      description:Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and a strong correlation between IL-15 and IL-17 levels in synovial fluid has been observed. IL-17 is a potent inducer of various cytokines such as tumor necrosis factor (TNF)-α, IL-1, and receptor activator of NF-κB ligand (RANKL). Additive or even synergistic effects with IL-1 and TNF-α in inducing cytokine expression and joint damage have been shown in vitro and in vivo. This review describes the role of IL-17 in the pathogenesis of destructive arthritis with a major focus on studies in vivo in arthritis models. From these studies in vivo it can be concluded that IL-17 becomes significant when T cells are a major element of the arthritis process. Moreover, IL-17 has the capacity to induce joint destruction in an IL-1-independent manner and can bypass TNF-dependent arthritis. Anti-IL-17 cytokine therapy is of interest as an additional new anti-rheumatic strategy for RA, in particular in situations in which elevated IL-17 might attenuate the response to anti-TNF/anti-IL-1 therapy.
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      dateModified:2004-11-30T00:00:00Z
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         autoimmune diseases
         cytokine
         inflammation
         interleukin-23
         osteoclast
         receptor activator of NF-κB ligand
         Rheumatology
         Orthopedics
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