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
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00281-019-00765-0.

Title:
Resolution of inflammation during multiple sclerosis | Seminars in Immunopathology
Description:
Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS). There are three clinical forms described: relapsing-remitting multiple sclerosis (RRMS), the most common initial presentation (85%) among which, if not treated, about half will transform, into the secondary progressive multiple sclerosis (SPMS) and the primary progressive MS (PPMS) (15%) that is directly progressive without superimposed clinical relapses. Inflammation is present in all subsets of MS. The relapsing/remitting form could represent itself a particular interest for the study of inflammation resolution even though it remains incomplete in MS. Successful resolution of acute inflammation is a highly regulated process and dependent on mechanisms engaged early in the inflammatory response that are scarcely studied in MS. Moreover, recent classes of disease-modifying treatment (DMTs) that are effective against RRMS act by re-establishing the inflammatory imbalance, taking advantage of the pre-existing endogenous suppressor. In this review, we will discuss the active role of regulatory immune cells in inflammation resolution as well as the role of tissue and non-hematopoietic cells as contributors to inflammation resolution. Finally, we will explore how DMTs, more specifically induction therapies, impact the resolution of inflammation during MS.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Health & Fitness
  • Education

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 7,626,432 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We find it hard to spot revenue streams.

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. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {πŸ”}

cells, pubmed, article, google, scholar, cas, central, cns, eae, multiple, sclerosis, inflammation, regulatory, cell, resolution, immune, immunol, patients, disease, tregs, astrocytes, inflammatory, role, autoimmune, increased, brain, function, system, antiinflammatory, mice, expression, treatment, lesions, mechanisms, macrophages, myelin, bbb, activated, suppressive, autoimmunity, fig, relapse, response, induction, diseases, barrier, experimental, encephalomyelitis, infiltration, nat,

Topics {βœ’οΈ}

tumour-necrosis-factor-related apoptosis-inducing ligand cd8+ hla-e-restricted show tnf-related apoptosis-induced ligand tnf-related apoptosis-inducing ligand tumor necrosis factor-alpha article download pdf astrocytes-endothelial cellular cross-talk e-series resolvin derived hla variant hla-drb115 lopez-diaz de cerio neurovascular unit pre-existing endogenous suppressor central nervous system peroxisome proliferator-activated receptor intrinsically immuno-suppressive nature dexamethasone-induced cell death dynamic cellular cross-talk gc-induced apoptosis due myeloid-derived suppressor cells cd46-mediated tr1 regulatory prototypical pro-inflammatory mediator pro-inflammatory cytokines tnfΞ± pro-resolving lipid mediators lineage-specification factor foxa1 nasal anti-cd3 administration qa-1-restricted cd8+ cells gp130-dependent astrocytic survival exaggerated pro-inflammatory response blood-derived myeloid cells clinically isolated syndrome pro-inflammatory gene expression trail/trail receptor system short-lived plasma blasts plp-specific tregs cells trail/trail-receptor pathway purely anti-inflammatory receptor pro-resolving nature illustrated selective pro-resolving gateway pro-resolving m2 macrophages activated myelin-specific cd4+ anti-inflammatory macrophage phenotype astrocytes trap t-cells pro-inflammatory cytokines il-12 anti-tnf-Ξ± antibodies foamy macrophage-suppressive mechanisms endogenous pro-resolutive mechanism placebo-controlled multicenter study high-dose corticosteroid medication paediatric-onset multiple sclerosis anti-inflammatory cytokines il-10

Questions {❓}

  • Robinson WH, Genovese MC, Moreland LW (2001) Demyelinating and neurologic events reported in association with tumor necrosis factor alpha antagonism: by what mechanisms could tumor necrosis factor alpha antagonists improve rheumatoid arthritis but exacerbate multiple sclerosis?
  • Trapp BD, Nave KA (2008) Multiple sclerosis: an immune or neurodegenerative disorder?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Resolution of inflammation during multiple sclerosis
         description:Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS). There are three clinical forms described: relapsing-remitting multiple sclerosis (RRMS), the most common initial presentation (85%) among which, if not treated, about half will transform, into the secondary progressive multiple sclerosis (SPMS) and the primary progressive MS (PPMS) (15%) that is directly progressive without superimposed clinical relapses. Inflammation is present in all subsets of MS. The relapsing/remitting form could represent itself a particular interest for the study of inflammation resolution even though it remains incomplete in MS. Successful resolution of acute inflammation is a highly regulated process and dependent on mechanisms engaged early in the inflammatory response that are scarcely studied in MS. Moreover, recent classes of disease-modifying treatment (DMTs) that are effective against RRMS act by re-establishing the inflammatory imbalance, taking advantage of the pre-existing endogenous suppressor. In this review, we will discuss the active role of regulatory immune cells in inflammation resolution as well as the role of tissue and non-hematopoietic cells as contributors to inflammation resolution. Finally, we will explore how DMTs, more specifically induction therapies, impact the resolution of inflammation during MS.
         datePublished:2019-11-15T00:00:00Z
         dateModified:2019-11-15T00:00:00Z
         pageStart:711
         pageEnd:726
         sameAs:https://doi.org/10.1007/s00281-019-00765-0
         keywords:
            Multiple sclerosis
            Suppressive immune cells
            Innate immune cells
            Neurovascular unit
            Astrocytes
            Blood-brain-barrier
            Induction therapies
            Immunology
            Internal Medicine
            Pathology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig2_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig3_HTML.png
         isPartOf:
            name:Seminars in Immunopathology
            issn:
               1863-2300
               1863-2297
            volumeNumber:41
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Berlin Heidelberg
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:F. Ruiz
               affiliation:
                     name:Lausanne University Hospital and University of Lausanne
                     address:
                        name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                        type:PostalAddress
                     type:Organization
               type:Person
               name:S. Vigne
               affiliation:
                     name:Lausanne University Hospital and University of Lausanne
                     address:
                        name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                        type:PostalAddress
                     type:Organization
               type:Person
               name:C. Pot
               url:http://orcid.org/0000-0002-1146-3129
               affiliation:
                     name:Lausanne University Hospital and University of Lausanne
                     address:
                        name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Resolution of inflammation during multiple sclerosis
      description:Multiple sclerosis (MS) is a frequent autoimmune demyelinating disease of the central nervous system (CNS). There are three clinical forms described: relapsing-remitting multiple sclerosis (RRMS), the most common initial presentation (85%) among which, if not treated, about half will transform, into the secondary progressive multiple sclerosis (SPMS) and the primary progressive MS (PPMS) (15%) that is directly progressive without superimposed clinical relapses. Inflammation is present in all subsets of MS. The relapsing/remitting form could represent itself a particular interest for the study of inflammation resolution even though it remains incomplete in MS. Successful resolution of acute inflammation is a highly regulated process and dependent on mechanisms engaged early in the inflammatory response that are scarcely studied in MS. Moreover, recent classes of disease-modifying treatment (DMTs) that are effective against RRMS act by re-establishing the inflammatory imbalance, taking advantage of the pre-existing endogenous suppressor. In this review, we will discuss the active role of regulatory immune cells in inflammation resolution as well as the role of tissue and non-hematopoietic cells as contributors to inflammation resolution. Finally, we will explore how DMTs, more specifically induction therapies, impact the resolution of inflammation during MS.
      datePublished:2019-11-15T00:00:00Z
      dateModified:2019-11-15T00:00:00Z
      pageStart:711
      pageEnd:726
      sameAs:https://doi.org/10.1007/s00281-019-00765-0
      keywords:
         Multiple sclerosis
         Suppressive immune cells
         Innate immune cells
         Neurovascular unit
         Astrocytes
         Blood-brain-barrier
         Induction therapies
         Immunology
         Internal Medicine
         Pathology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig2_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00281-019-00765-0/MediaObjects/281_2019_765_Fig3_HTML.png
      isPartOf:
         name:Seminars in Immunopathology
         issn:
            1863-2300
            1863-2297
         volumeNumber:41
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Berlin Heidelberg
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:F. Ruiz
            affiliation:
                  name:Lausanne University Hospital and University of Lausanne
                  address:
                     name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                     type:PostalAddress
                  type:Organization
            type:Person
            name:S. Vigne
            affiliation:
                  name:Lausanne University Hospital and University of Lausanne
                  address:
                     name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                     type:PostalAddress
                  type:Organization
            type:Person
            name:C. Pot
            url:http://orcid.org/0000-0002-1146-3129
            affiliation:
                  name:Lausanne University Hospital and University of Lausanne
                  address:
                     name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Seminars in Immunopathology
      issn:
         1863-2300
         1863-2297
      volumeNumber:41
Organization:
      name:Springer Berlin Heidelberg
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Lausanne University Hospital and University of Lausanne
      address:
         name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
         type:PostalAddress
      name:Lausanne University Hospital and University of Lausanne
      address:
         name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
         type:PostalAddress
      name:Lausanne University Hospital and University of Lausanne
      address:
         name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:F. Ruiz
      affiliation:
            name:Lausanne University Hospital and University of Lausanne
            address:
               name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
               type:PostalAddress
            type:Organization
      name:S. Vigne
      affiliation:
            name:Lausanne University Hospital and University of Lausanne
            address:
               name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
               type:PostalAddress
            type:Organization
      name:C. Pot
      url:http://orcid.org/0000-0002-1146-3129
      affiliation:
            name:Lausanne University Hospital and University of Lausanne
            address:
               name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
      name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland
      name:Laboratories of Neuroimmunology, Neuroscience Research Center and Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Epalinges, Switzerland

External Links {πŸ”—}(519)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Foundation
  • Prism.js

CDN Services {πŸ“¦}

  • Crossref

5.5s.