Here's how LINK.SPRINGER.COM makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

LINK . SPRINGER . COM {}

  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
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries

We are analyzing https://link.springer.com/article/10.1186/ar3736.

Title:
Interleukin-10 produced by B cells is crucial for the suppression of Th17/Th1 responses, induction of T regulatory type 1 cells and reduction of collagen-induced arthritis | Arthritis Research & Therapy
Description:
Introduction Interleukin-10 (IL-10) producing B cells, also known as regulatory B (Breg) cells, play a key role in controlling autoimmunity. Our laboratory and others have demonstrated a pivotal role for Bregs in rheumatological disorders, including experimental models of arthritis and lupus. The aim of this study was to identify the role of endogenous IL-10 secreting B cells in vivo in controlling the induction and disease progression of collagen-induced arthritis (CIA). Methods We generated chimeric mice that had IL-10 knocked-out specifically in the B cell population. These mice were compared with wild-type (WT) B cell chimeric mice for their susceptibility to CIA. Results Here we report that chimeric mice specifically lacking IL-10 producing B cells (IL-10-/- B cell) developed an exacerbated CIA compared to chimeric wild type B cell (WT B cell) mice. A marked increase in inflammatory Th1 and Th17 cells were detected in IL-10-/-B cell mice compared to WT B cell mice. Furthermore, there was a reduction in IL-10 secreting CD4+ Tr1 cells in these animals. Conclusions IL-10 producing B cells restrain inflammation by promoting differentiation of immuno-regulatory over pro-inflammatory T cells and, hence, act to maintain tolerance.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

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? {💸}

The income method remains a mystery to us.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

cells, mice, cell, pubmed, arthritis, article, google, scholar, cas, data, regulatory, cia, disease, compared, animals, figure, immunol, experimental, analysis, shown, cytokine, ifnγ, central, type, experiments, role, chimeric, inflammation, increased, levels, collageninduced, vivo, development, interleukin, exacerbated, bone, hours, collagen, foxp, mauri, joint, μmt, aia, numbers, file, sem, tregs, induction, number, producing,

Topics {✒️}

administered biotin-anti-ifnγ-labelled antibodies cytokine-biotin-anti-cytokine mab complexes produce anti-collagen antibodies article download pdf anti-mouse il-10 apc b-cell-derived il-10 specific pathogen-free conditions anti-cd4 fitc mab th1/th2 cytokine patterns potent pro-inflammatory cytokines antigen-induced experimental arthritis increased pro-inflammatory cytokines severe collagen-induced arthritis pro-inflammatory th1 cytokines antigen-mediated joint swelling 50 ng/ml sigma-aldrich 500 ng/ml sigma-aldrich full size image cd25+cd4+ tr cells rosser & claudia mauri type ii collagen il-10-reporter expressing regulatory article number r32 cytokine flowcytomix kit cell-dependent inflammatory responses protease-activated receptor 2 compared foxp3+treg numbers anti-foxp3 mab antigen induced arthritis antigen-induced arthritis immune-regulatory tr1 cells privacy choices/manage cookies draining lymph node systemic experimental arthritis pro-inflammatory cytokines springer semin immunopathol evans jg cytokine gene activation home office anti-cd3 antibody chimeric wild type cell-derived il-10 results bone marrow preparations bone marrow consisting host bone marrow intracellular cytokine staining increased intestinal-gas collagen-induced arthritis pro-inflammatory th1 anti-mbsa antibodies

Questions {❓}

  • Mauri C, Carter N: Is there a feudal hierarchy amongst regulatory immune cells?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Interleukin-10 produced by B cells is crucial for the suppression of Th17/Th1 responses, induction of T regulatory type 1 cells and reduction of collagen-induced arthritis
         description:Interleukin-10 (IL-10) producing B cells, also known as regulatory B (Breg) cells, play a key role in controlling autoimmunity. Our laboratory and others have demonstrated a pivotal role for Bregs in rheumatological disorders, including experimental models of arthritis and lupus. The aim of this study was to identify the role of endogenous IL-10 secreting B cells in vivo in controlling the induction and disease progression of collagen-induced arthritis (CIA). We generated chimeric mice that had IL-10 knocked-out specifically in the B cell population. These mice were compared with wild-type (WT) B cell chimeric mice for their susceptibility to CIA. Here we report that chimeric mice specifically lacking IL-10 producing B cells (IL-10-/- B cell) developed an exacerbated CIA compared to chimeric wild type B cell (WT B cell) mice. A marked increase in inflammatory Th1 and Th17 cells were detected in IL-10-/-B cell mice compared to WT B cell mice. Furthermore, there was a reduction in IL-10 secreting CD4+ Tr1 cells in these animals. IL-10 producing B cells restrain inflammation by promoting differentiation of immuno-regulatory over pro-inflammatory T cells and, hence, act to maintain tolerance.
         datePublished:2012-02-08T00:00:00Z
         dateModified:2012-02-08T00:00:00Z
         pageStart:1
         pageEnd:9
         license:http://creativecommons.org/licenses/by/2.0/
         sameAs:https://doi.org/10.1186/ar3736
         keywords:
            Cell Mouse
            Chimeric Mouse
            Experimental Arthritis
            Antigen Induce Arthritis
            Treg Number
            Rheumatology
            Orthopedics
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig3_HTML.jpg
         isPartOf:
            name:Arthritis Research & Therapy
            issn:
               1478-6354
            volumeNumber:14
            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:Natalie A Carter
               affiliation:
                     name:University College London
                     address:
                        name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Elizabeth C Rosser
               affiliation:
                     name:University College London
                     address:
                        name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Claudia Mauri
               affiliation:
                     name:University College London
                     address:
                        name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Interleukin-10 produced by B cells is crucial for the suppression of Th17/Th1 responses, induction of T regulatory type 1 cells and reduction of collagen-induced arthritis
      description:Interleukin-10 (IL-10) producing B cells, also known as regulatory B (Breg) cells, play a key role in controlling autoimmunity. Our laboratory and others have demonstrated a pivotal role for Bregs in rheumatological disorders, including experimental models of arthritis and lupus. The aim of this study was to identify the role of endogenous IL-10 secreting B cells in vivo in controlling the induction and disease progression of collagen-induced arthritis (CIA). We generated chimeric mice that had IL-10 knocked-out specifically in the B cell population. These mice were compared with wild-type (WT) B cell chimeric mice for their susceptibility to CIA. Here we report that chimeric mice specifically lacking IL-10 producing B cells (IL-10-/- B cell) developed an exacerbated CIA compared to chimeric wild type B cell (WT B cell) mice. A marked increase in inflammatory Th1 and Th17 cells were detected in IL-10-/-B cell mice compared to WT B cell mice. Furthermore, there was a reduction in IL-10 secreting CD4+ Tr1 cells in these animals. IL-10 producing B cells restrain inflammation by promoting differentiation of immuno-regulatory over pro-inflammatory T cells and, hence, act to maintain tolerance.
      datePublished:2012-02-08T00:00:00Z
      dateModified:2012-02-08T00:00:00Z
      pageStart:1
      pageEnd:9
      license:http://creativecommons.org/licenses/by/2.0/
      sameAs:https://doi.org/10.1186/ar3736
      keywords:
         Cell Mouse
         Chimeric Mouse
         Experimental Arthritis
         Antigen Induce Arthritis
         Treg Number
         Rheumatology
         Orthopedics
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Far3736/MediaObjects/13075_2011_Article_3458_Fig3_HTML.jpg
      isPartOf:
         name:Arthritis Research & Therapy
         issn:
            1478-6354
         volumeNumber:14
         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:Natalie A Carter
            affiliation:
                  name:University College London
                  address:
                     name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Elizabeth C Rosser
            affiliation:
                  name:University College London
                  address:
                     name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Claudia Mauri
            affiliation:
                  name:University College London
                  address:
                     name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Arthritis Research & Therapy
      issn:
         1478-6354
      volumeNumber:14
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University College London
      address:
         name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
         type:PostalAddress
      name:University College London
      address:
         name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
         type:PostalAddress
      name:University College London
      address:
         name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Natalie A Carter
      affiliation:
            name:University College London
            address:
               name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Elizabeth C Rosser
      affiliation:
            name:University College London
            address:
               name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
               type:PostalAddress
            type:Organization
      name:Claudia Mauri
      affiliation:
            name:University College London
            address:
               name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
      name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK
      name:Centre for Rheumatology Research, Division of Medicine, University College London, London, UK

External Links {🔗}(187)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

5.12s.