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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/10.1007/s00018-012-1058-6.

Title:
Regulatory T cells, mTOR kinase, and metabolic activity | Cellular and Molecular Life Sciences
Description:
The field that links immunity and metabolism is rapidly expanding. Apparently, non-immunological disorders such as obesity and type 2 diabetes have been linked to immune dysregulation, suggesting that metabolic alterations can be induced by or be a consequence of an altered self-immune tolerance. In this context, a key role is played by signaling systems acting as metabolic “sensors” linking energy/nutritional status to regulatory T (Treg) cell functions. We propose that a dynamic/oscillatory activity of intracellular metabolism, through mTOR modulation, might represent a shift in understanding the molecular mechanisms governing Treg cell tolerance. In particular, the decision between Treg cell proliferation and hyporesponsiveness arises from their ability to probe the extracellular milieu and, modulating the metabolic intracellular signaling, to determine different qualitative and quantitative functional outcomes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

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.

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

We can't tell how the site generates income.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

article, google, scholar, cas, pubmed, cells, cell, regulatory, immunol, mtor, metabolic, immunity, rapamycin, matarese, metabolism, nat, med, kinase, immune, signaling, differentiation, procaccini, tolerance, foxp, sci, regulates, biol, nature, mol, function, treg, memory, blood, diabetes, role, activation, glucose, tcell, control, regulation, development, mammalian, target, sabatini, dendritic, acad, wang, activity, giuseppe, autoimmune,

Topics {✒️}

viral-specific cd8 + tcell responses month download article/chapter naturally-occurring cd4+cd25+ immunoregulatory requires cd28-mediated akt-dependent functional cd4+cd25+foxp3+ regulatory nutrient/energy-sensing mammalian target peripheral cd4+cd25+foxp3+ regulatory brain-derived neurotrophic factor rapamycin augments pathogen-specific reverses starvation-induced immunosuppression sin1-mtorc2 suppresses rag transcription factors t-bet cd4+cd25+foxp3+ regulatory noninsulin-dependent diabetes mellitus anti-inflammatory cytokines il-10 t-cell immune response interleukin-2 receptor signaling regulatory t-cell differentiation cell-mediated immune suppression regulatory cell-mediated suppression full article pdf naturally occurring regulatory glycolytic energy production kinase mtor regulates giuseppe matarese naturally occurring population regulatory t-cell immunity privacy choices/manage cookies cd4+cd25+ immunoregulatory article procaccini graft-reactive cd8+ foxp3-dependent programme cd4+cd25+ regulatory rapamycin signaling pathway pd-l1 regulates related subjects t-cell response energy metabolism nutrient-sensitive complex adipocentric view hypoxia-inducible factor 1 foxp3-mediated induction facoltà di medicina dipartimento di biologia metabolic intracellular signaling innate inflammatory response feto-maternal tolerance foxp3+ natural regulatory quantitative functional outcomes june ch

Questions {❓}

  • Yang X, Smith U (2007) Adipose tissue distribution and risk of metabolic disease: does thiazolidinedione-induced adipose tissue redistribution provide a clue to the answer?

Schema {🗺️}

WebPage:
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         headline:Regulatory T cells, mTOR kinase, and metabolic activity
         description:The field that links immunity and metabolism is rapidly expanding. Apparently, non-immunological disorders such as obesity and type 2 diabetes have been linked to immune dysregulation, suggesting that metabolic alterations can be induced by or be a consequence of an altered self-immune tolerance. In this context, a key role is played by signaling systems acting as metabolic “sensors” linking energy/nutritional status to regulatory T (Treg) cell functions. We propose that a dynamic/oscillatory activity of intracellular metabolism, through mTOR modulation, might represent a shift in understanding the molecular mechanisms governing Treg cell tolerance. In particular, the decision between Treg cell proliferation and hyporesponsiveness arises from their ability to probe the extracellular milieu and, modulating the metabolic intracellular signaling, to determine different qualitative and quantitative functional outcomes.
         datePublished:2012-07-04T00:00:00Z
         dateModified:2012-07-04T00:00:00Z
         pageStart:3975
         pageEnd:3987
         sameAs:https://doi.org/10.1007/s00018-012-1058-6
         keywords:
            Metabolism
            Immune tolerance
            mTOR
            Treg cells
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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         isPartOf:
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            issn:
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            volumeNumber:69
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      headline:Regulatory T cells, mTOR kinase, and metabolic activity
      description:The field that links immunity and metabolism is rapidly expanding. Apparently, non-immunological disorders such as obesity and type 2 diabetes have been linked to immune dysregulation, suggesting that metabolic alterations can be induced by or be a consequence of an altered self-immune tolerance. In this context, a key role is played by signaling systems acting as metabolic “sensors” linking energy/nutritional status to regulatory T (Treg) cell functions. We propose that a dynamic/oscillatory activity of intracellular metabolism, through mTOR modulation, might represent a shift in understanding the molecular mechanisms governing Treg cell tolerance. In particular, the decision between Treg cell proliferation and hyporesponsiveness arises from their ability to probe the extracellular milieu and, modulating the metabolic intracellular signaling, to determine different qualitative and quantitative functional outcomes.
      datePublished:2012-07-04T00:00:00Z
      dateModified:2012-07-04T00:00:00Z
      pageStart:3975
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      sameAs:https://doi.org/10.1007/s00018-012-1058-6
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         Metabolism
         Immune tolerance
         mTOR
         Treg cells
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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            address:
               name:Dipartimento di Medicina, FacoltĂ  di Medicina, UniversitĂ  di Salerno, Baronissi, Italy
               type:PostalAddress
            type:Organization
            name:Consiglio Nazionale delle Ricerche (IEOS-CNR)
            address:
               name:Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples, Italy
               type:PostalAddress
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            address:
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      name:c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, UniversitĂ  di Napoli ‘‘Federico II”, Naples, Italy
      name:Dipartimento di Medicina, FacoltĂ  di Medicina, UniversitĂ  di Salerno, Baronissi, Italy
      name:Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples, Italy
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External Links {🔗}(404)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

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