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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Health & Fitness
Education
Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

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 {🗺️}

WebPage:
      mainEntity:
         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.
         datePublished:2004-11-30T00:00:00Z
         dateModified:2004-11-30T00:00:00Z
         pageStart:1
         pageEnd:9
         sameAs:https://doi.org/10.1186/ar1478
         keywords:
            autoimmune diseases
            cytokine
            inflammation
            interleukin-23
            osteoclast
            receptor activator of NF-κB ligand
            Rheumatology
            Orthopedics
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far1478/MediaObjects/13075_2004_Article_1359_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far1478/MediaObjects/13075_2004_Article_1359_Fig2_HTML.jpg
         isPartOf:
            name:Arthritis Res Ther
            issn:
               1478-6354
            volumeNumber:7
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Erik Lubberts
               affiliation:
                     name:University Medical Center Nijmegen
                     address:
                        name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Marije I Koenders
               affiliation:
                     name:University Medical Center Nijmegen
                     address:
                        name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Wim B van den Berg
               affiliation:
                     name:University Medical Center Nijmegen
                     address:
                        name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      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.
      datePublished:2004-11-30T00:00:00Z
      dateModified:2004-11-30T00:00:00Z
      pageStart:1
      pageEnd:9
      sameAs:https://doi.org/10.1186/ar1478
      keywords:
         autoimmune diseases
         cytokine
         inflammation
         interleukin-23
         osteoclast
         receptor activator of NF-κB ligand
         Rheumatology
         Orthopedics
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far1478/MediaObjects/13075_2004_Article_1359_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far1478/MediaObjects/13075_2004_Article_1359_Fig2_HTML.jpg
      isPartOf:
         name:Arthritis Res Ther
         issn:
            1478-6354
         volumeNumber:7
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Erik Lubberts
            affiliation:
                  name:University Medical Center Nijmegen
                  address:
                     name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Marije I Koenders
            affiliation:
                  name:University Medical Center Nijmegen
                  address:
                     name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Wim B van den Berg
            affiliation:
                  name:University Medical Center Nijmegen
                  address:
                     name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Arthritis Res Ther
      issn:
         1478-6354
      volumeNumber:7
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University Medical Center Nijmegen
      address:
         name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
         type:PostalAddress
      name:University Medical Center Nijmegen
      address:
         name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
         type:PostalAddress
      name:University Medical Center Nijmegen
      address:
         name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Erik Lubberts
      affiliation:
            name:University Medical Center Nijmegen
            address:
               name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Marije I Koenders
      affiliation:
            name:University Medical Center Nijmegen
            address:
               name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Wim B van den Berg
      affiliation:
            name:University Medical Center Nijmegen
            address:
               name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
      name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands
      name:Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands

External Links {🔗}(264)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.24s.

LINK . SPRINGER . COM {}