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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. Social Networks
  11. External Links
  12. Analytics And Tracking
  13. Libraries
  14. Hosting Providers
  15. CDN Services

We began analyzing https://www.nature.com/articles/nri3707, but it redirected us to https://www.nature.com/articles/nri3707. The analysis below is for the second page.

Title[redir]:
The IL-23–IL-17 immune axis: from mechanisms to therapeutic testing | Nature Reviews Immunology
Description:
T helper 17 (TH17) cells promote protective immune responses against infection, particularly at barrier sites, but they can also have pathogenic roles in inflammatory diseases. In this Review, the authors describe the factors that control the development and maintenance of TH17 cells, and discuss their diverse functions in both health and disease. Following the discovery of T helper 17 (TH17) cells, the past decade has witnessed a major revision of the TH subset paradigm and substantial progress has been made in deciphering the molecular mechanisms of T cell lineage commitment and function. In this Review, we focus on the recent advances that have been made regarding the transcriptional control of TH17 cell plasticity and stability, as well as the effector functions of TH17 cells, and we highlight the mechanisms of IL-17 signalling in mesenchymal and barrier epithelial tissues. We also discuss the emerging clinical data showing that IL-17-specific and IL-23-specific antibody treatments are remarkably effective for treating many immune-mediated inflammatory diseases.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org 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.
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How Does Doi.org Make Money? {💸}

The income method remains a mystery to us.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

pubmed, article, google, scholar, cas, nature, central, cells, immunol, cell, interleukin, immunity, autoimmune, inflammation, inflammatory, receptor, med, disease, helper, factor, differentiation, psoriasis, signaling, rev, transcription, cytokine, human, lineage, signal, exp, chronic, signalling, study, function, rorγt, act, stat, candidiasis, gaffen, regulatory, content, mechanisms, transforming, growth, protein, regulation, access, biol, essential, cua,

Topics {✒️}

ubiquitin-editing enzyme a20 permissions reprints late-breaking research symposium privacy policy nature portfolio received research grants advertising il-17-induced nf-κb activation mitogen-activated protein kinases interferon-γ-expressing th17 cells social media il-17ra-specific antibody therapy transforming growth factor-β author information authors il-17-induced act1-mediated cxcl1 il-17r-mediated signalling axis ubiquitin-specific protease usp25 double-blind placebo-controlled trial selective nf-κb activation il-23-specific antibody treatments ccaat/enhancer-binding proteins erk1/2-dependent nf-κb anti-interleukin-17-receptor antibody siderophore-mediated iron acquisition pre-existent enhancer landscape tumor necrosis factor-α genome-wide association study anti-il-17 mabs herald author correspondence single-stranded rna molecules splicing-regulatory factor sf2 scfβ-trcp-mediated degradation conserved sef/il-17r card15/nod2 mutational analysis inherited il-12p40 deficiency tnf-α-induced genes mediating il-25-induced activities immune-mediated inflammatory diseases aryl hydrocarbon receptor dual-specificity phosphatases 22-deficient cell-dependent iga responses il-23–il-17 immune axis il-23-induced il-17 production ankylosing spondylitis identifies springerlink instant access il-17f-induced effects permissions il-17r signalling pathway il17a fate-mapping strategy personal data

Questions {❓}

  • Master regulators or lineage-specifying?

Schema {🗺️}

WebPage:
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         headline:The IL-23–IL-17 immune axis: from mechanisms to therapeutic testing
         description: T helper 17 (TH17) cells promote protective immune responses against infection, particularly at barrier sites, but they can also have pathogenic roles in inflammatory diseases. In this Review, the authors describe the factors that control the development and maintenance of TH17 cells, and discuss their diverse functions in both health and disease. Following the discovery of T helper 17 (TH17) cells, the past decade has witnessed a major revision of the TH subset paradigm and substantial progress has been made in deciphering the molecular mechanisms of T cell lineage commitment and function. In this Review, we focus on the recent advances that have been made regarding the transcriptional control of TH17 cell plasticity and stability, as well as the effector functions of TH17 cells, and we highlight the mechanisms of IL-17 signalling in mesenchymal and barrier epithelial tissues. We also discuss the emerging clinical data showing that IL-17-specific and IL-23-specific antibody treatments are remarkably effective for treating many immune-mediated inflammatory diseases.
         datePublished:2014-08-22T00:00:00Z
         dateModified:2014-08-22T00:00:00Z
         pageStart:585
         pageEnd:600
         sameAs:https://doi.org/10.1038/nri3707
         keywords:
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            Interleukins
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      headline:The IL-23–IL-17 immune axis: from mechanisms to therapeutic testing
      description: T helper 17 (TH17) cells promote protective immune responses against infection, particularly at barrier sites, but they can also have pathogenic roles in inflammatory diseases. In this Review, the authors describe the factors that control the development and maintenance of TH17 cells, and discuss their diverse functions in both health and disease. Following the discovery of T helper 17 (TH17) cells, the past decade has witnessed a major revision of the TH subset paradigm and substantial progress has been made in deciphering the molecular mechanisms of T cell lineage commitment and function. In this Review, we focus on the recent advances that have been made regarding the transcriptional control of TH17 cell plasticity and stability, as well as the effector functions of TH17 cells, and we highlight the mechanisms of IL-17 signalling in mesenchymal and barrier epithelial tissues. We also discuss the emerging clinical data showing that IL-17-specific and IL-23-specific antibody treatments are remarkably effective for treating many immune-mediated inflammatory diseases.
      datePublished:2014-08-22T00:00:00Z
      dateModified:2014-08-22T00:00:00Z
      pageStart:585
      pageEnd:600
      sameAs:https://doi.org/10.1038/nri3707
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         Interleukins
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         Biomedicine
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         name:Merck Research Laboratories, Palo Alto, Palo Alto, USA
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         name:Division of Rheumatology and Clinical Immunology, Pittsburgh, USA
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               type:PostalAddress
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      name:Abhishek V. Garg
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            name:Division of Rheumatology and Clinical Immunology
            address:
               name:Division of Rheumatology and Clinical Immunology, Pittsburgh, USA
               type:PostalAddress
            type:Organization
      name:Daniel J. Cua
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            name:Merck Research Laboratories, Palo Alto
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External Links {🔗}(695)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

4.77s.