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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s00281-019-00733-8.

Title:
The pathogenicity of Th17 cells in autoimmune diseases | Seminars in Immunopathology
Description:
IL-17-producing T helper (Th17) cells have been implicated in the pathogenesis of many inflammatory and autoimmune diseases. Targeting the effector cytokines IL-17 and GM-CSF secreted by autoimmune Th17 cells has been shown to be effective for the treatment of the diseases. Understanding a molecular basis of Th17 differentiation and effector functions is therefore critical for the regulation of the pathogenicity of tissue Th17 cells in chronic inflammation. Here, we discuss the roles of proinflammatory cytokines and environmental stimuli in the control of Th17 differentiation and chronic tissue inflammation by pathogenic Th17 cells in humans and in mouse models of autoimmune diseases. We also highlight recent advances in the regulation of pathogenic Th17 cells by gut microbiota and immunometabolism in autoimmune arthritis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

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 {πŸ“ˆ}

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.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We can't see how the site brings in money.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {πŸ”}

pubmed, article, google, scholar, cas, arthritis, cells, central, rheumatoid, cell, autoimmune, immunol, nat, rheum, sakaguchi, nature, med, chen, patients, interleukin, httpsdoiorgni, hirota, helper, differentiation, wang, gmcsf, receptor, cytokine, exp, httpsdoiorgjem, httpsdoiorgart, study, factor, lee, phase, human, httpsdoiorgnature, yang, synovial, inflammatory, expression, immunity, pathogenicity, inflammation, pathogenic, cua, induction, ito, diseases, effector,

Topics {βœ’οΈ}

granulocyte-macrophage colony-stimulating factor anti-interleukin-17a monoclonal antibody cell-specific stat3-deficient mice month download article/chapter il-1/il-1r antagonist system meyer zu horste transforming growth factor-beta gm-csf mediates autoimmunity tumor necrosis factor-alpha anti-interleukin-17 monoclonal antibody van der horst-bruinsma segmented filamentous bacteria t-cell programs cyclosporin a-sensitive mechanism cytokine gm-csf drives human leukocyte antigen-drb1 aryl hydrocarbon receptor il-23-il-17 immune axis full article pdf interleukin-6/interleukin-17 cytokine axis cell-dependent iga responses collagen-induced arthritis human monoclonal antibody ccr6-expressing th17 cells transcription factor activities epidermal growth factor phase ib/iia randomised il-23-induced production hypoxia-inducible factor 1 harrington le hyper-ige syndrome open-label study van der heijde gm-csf production induces autoimmune inflammation gonzalez-gay ma rorgammat drives production quintana fj mediate autoimmune encephalomyelitis experimental autoimmune encephalomyelitis nuclear receptor rorgammat stat transcription factors privacy choices/manage cookies cytokine gm-csf 17 cell-mediated pathology burmester gr al-aama jy firestein gs gm-csf secreted gm-csf affects

Questions {❓}

  • Firestein GS, Zvaifler NJ (1990) How important are T cells in chronic rheumatoid synovitis?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:The pathogenicity of Th17 cells in autoimmune diseases
         description:IL-17-producing T helper (Th17) cells have been implicated in the pathogenesis of many inflammatory and autoimmune diseases. Targeting the effector cytokines IL-17 and GM-CSF secreted by autoimmune Th17 cells has been shown to be effective for the treatment of the diseases. Understanding a molecular basis of Th17 differentiation and effector functions is therefore critical for the regulation of the pathogenicity of tissue Th17 cells in chronic inflammation. Here, we discuss the roles of proinflammatory cytokines and environmental stimuli in the control of Th17 differentiation and chronic tissue inflammation by pathogenic Th17 cells in humans and in mouse models of autoimmune diseases. We also highlight recent advances in the regulation of pathogenic Th17 cells by gut microbiota and immunometabolism in autoimmune arthritis.
         datePublished:2019-03-19T00:00:00Z
         dateModified:2019-04-29T00:00:00Z
         pageStart:283
         pageEnd:297
         sameAs:https://doi.org/10.1007/s00281-019-00733-8
         keywords:
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            GM-CSF
            Th17 cells
            Autoimmune arthritis
            EAE
            Rheumatoid arthritis
            Immunology
            Internal Medicine
            Pathology
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         isPartOf:
            name:Seminars in Immunopathology
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      headline:The pathogenicity of Th17 cells in autoimmune diseases
      description:IL-17-producing T helper (Th17) cells have been implicated in the pathogenesis of many inflammatory and autoimmune diseases. Targeting the effector cytokines IL-17 and GM-CSF secreted by autoimmune Th17 cells has been shown to be effective for the treatment of the diseases. Understanding a molecular basis of Th17 differentiation and effector functions is therefore critical for the regulation of the pathogenicity of tissue Th17 cells in chronic inflammation. Here, we discuss the roles of proinflammatory cytokines and environmental stimuli in the control of Th17 differentiation and chronic tissue inflammation by pathogenic Th17 cells in humans and in mouse models of autoimmune diseases. We also highlight recent advances in the regulation of pathogenic Th17 cells by gut microbiota and immunometabolism in autoimmune arthritis.
      datePublished:2019-03-19T00:00:00Z
      dateModified:2019-04-29T00:00:00Z
      pageStart:283
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      sameAs:https://doi.org/10.1007/s00281-019-00733-8
      keywords:
         IL-17
         GM-CSF
         Th17 cells
         Autoimmune arthritis
         EAE
         Rheumatoid arthritis
         Immunology
         Internal Medicine
         Pathology
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                     name:Department of Nephrology, Graduate School of Medicine, Osaka University, Osaka, Japan
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            name:Yusuke Takeuchi
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            name:Keiji Hirota
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         name:Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
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         name:Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
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            address:
               name:Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
               type:PostalAddress
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            name:Osaka University
            address:
               name:Department of Nephrology, Graduate School of Medicine, Osaka University, Osaka, Japan
               type:PostalAddress
            type:Organization
      name:Yusuke Takeuchi
      affiliation:
            name:Kyoto University
            address:
               name:Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
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      name:Keiji Hirota
      affiliation:
            name:Kyoto University
            address:
               name:Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
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      name:Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
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