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. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s10495-010-0472-1.

Title:
Dangerous attraction: phagocyte recruitment and danger signals of apoptotic and necrotic cells | Apoptosis
Description:
Tissue homeostasis in metazoa requires the rapid and efficient clearance of dying cells by professional or semi-professional phagocytes. Impairment of this finely regulated, fundamental process has been implicated in the development of autoimmune diseases, such as systemic lupus erythematosus. Various studies have provided us a detailed understanding of the interaction between dying cells and phagocytes as well as the current concept that apoptotic cell removal leads to a non- or anti-inflammatory response, whereas necrotic cell removal stimulates a pro-inflammatory reaction. In contrast, our knowledge about the soluble factors released from dying cells is rather limited, although meanwhile it is generally accepted that not only the dying cell itself but also the substances liberated during cell death contribute to the process of corpse clearance and the subsequent immune response. This review article is intended as an up-to-date survey over attraction and danger signals of apoptotic, primary and secondary necrotic cells, their function as chemoattractants in phagocyte recruitment, additional effects on the immune system, and the receptors, which are engaged in this scenario.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

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.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We see no obvious way the site makes money.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

google, scholar, pubmed, cas, article, cell, cells, protein, immunol, biol, receptor, apoptotic, human, chem, arthritis, release, factor, activation, apoptosis, dendritic, inflammation, death, heat, shock, blood, med, extracellular, proteins, immune, rheum, hmgb, cytokine, proinflammatory, receptors, macrophages, yamamoto, induces, expression, atp, signals, polypeptide, urate, necrosis, wang, exp, nat, yang, clearance, wesselborg, systemic,

Topics {βœ’οΈ}

nuclear factor kappa-light-chain-enhancer n-formylmethionyl-leucyl-phenylalanine gp96 fractalkine-induced mfg-e8 leads gi/o-coupled p2y receptors month download article/chapter hepatoma-derived growth factor heat shock protein-based class ii-restricted epitopes normal t-cell expressed il-6/sil-6r complex itam-coupled activating receptor ionizing radiation-induced apoptosis p2x7/p2z purinoreceptor-mediated activation mammalian multi-synthetase complex shear stress-induced [ca2+] chemokine/chemokine-receptor family mfg-e8-deficient mice vitamin d-binding protein reduction/oxidation regulate immunity heparin-binding domain lead human aminoacyl-trna synthetase monocyte chemotactic factor calcium-binding protein mrp-14 antiapoptotic mediator sphingosine-1-phosphate lps-induced cytokine production late-onset autoimmune syndrome tumor-derived polypeptide activates host-response mechanisms s19 ribosomal protein iron-binding protein lactoferrin nk/idc interaction results vesicle-mediated secretory pathway proinflammatory protein s100a8/a9 cpg motif-independent activation crystal-induced inflammation professional antigen-presenting cells monosodium urate crystals transcription factor nfat full article pdf article apoptosis aims heat shock proteins proinflammatory trans-signaling function myeloid-related protein s100 protein cp-10 apoptosis induces expression heat induced release activating dendritic cells atp-induced chemotaxis tumor-derived cytokine serotonergic growth factor

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Dangerous attraction: phagocyte recruitment and danger signals of apoptotic and necrotic cells
         description:Tissue homeostasis in metazoa requires the rapid and efficient clearance of dying cells by professional or semi-professional phagocytes. Impairment of this finely regulated, fundamental process has been implicated in the development of autoimmune diseases, such as systemic lupus erythematosus. Various studies have provided us a detailed understanding of the interaction between dying cells and phagocytes as well as the current concept that apoptotic cell removal leads to a non- or anti-inflammatory response, whereas necrotic cell removal stimulates a pro-inflammatory reaction. In contrast, our knowledge about the soluble factors released from dying cells is rather limited, although meanwhile it is generally accepted that not only the dying cell itself but also the substances liberated during cell death contribute to the process of corpse clearance and the subsequent immune response. This review article is intended as an up-to-date survey over attraction and danger signals of apoptotic, primary and secondary necrotic cells, their function as chemoattractants in phagocyte recruitment, additional effects on the immune system, and the receptors, which are engaged in this scenario.
         datePublished:2010-02-16T00:00:00Z
         dateModified:2010-02-16T00:00:00Z
         pageStart:1007
         pageEnd:1028
         sameAs:https://doi.org/10.1007/s10495-010-0472-1
         keywords:
            Apoptosis
            Necrosis
            Phagocytosis
            Engulfment
            Migration
            Chemotaxis
            β€˜Find-me’ signals
            Attraction signals
            Danger signals
            DAMPs
            Cancer Research
            Cell Biology
            Oncology
            Biochemistry
            general
            Virology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig3_HTML.gif
         isPartOf:
            name:Apoptosis
            issn:
               1573-675X
               1360-8185
            volumeNumber:15
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Christoph Peter
               affiliation:
                     name:University of Tuebingen
                     address:
                        name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Sebastian Wesselborg
               affiliation:
                     name:University of Tuebingen
                     address:
                        name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Martin Herrmann
               affiliation:
                     name:University Hospital Erlangen
                     address:
                        name:Institute for Clinical Immunology, Department for Internal Medicine 3, University Hospital Erlangen, Erlangen, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Kirsten Lauber
               affiliation:
                     name:University of Tuebingen
                     address:
                        name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                        type:PostalAddress
                     type:Organization
                     name:Eberhard-Karls-University
                     address:
                        name:Department of Internal Medicine I, Eberhard-Karls-University, Tuebingen, Germany
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Dangerous attraction: phagocyte recruitment and danger signals of apoptotic and necrotic cells
      description:Tissue homeostasis in metazoa requires the rapid and efficient clearance of dying cells by professional or semi-professional phagocytes. Impairment of this finely regulated, fundamental process has been implicated in the development of autoimmune diseases, such as systemic lupus erythematosus. Various studies have provided us a detailed understanding of the interaction between dying cells and phagocytes as well as the current concept that apoptotic cell removal leads to a non- or anti-inflammatory response, whereas necrotic cell removal stimulates a pro-inflammatory reaction. In contrast, our knowledge about the soluble factors released from dying cells is rather limited, although meanwhile it is generally accepted that not only the dying cell itself but also the substances liberated during cell death contribute to the process of corpse clearance and the subsequent immune response. This review article is intended as an up-to-date survey over attraction and danger signals of apoptotic, primary and secondary necrotic cells, their function as chemoattractants in phagocyte recruitment, additional effects on the immune system, and the receptors, which are engaged in this scenario.
      datePublished:2010-02-16T00:00:00Z
      dateModified:2010-02-16T00:00:00Z
      pageStart:1007
      pageEnd:1028
      sameAs:https://doi.org/10.1007/s10495-010-0472-1
      keywords:
         Apoptosis
         Necrosis
         Phagocytosis
         Engulfment
         Migration
         Chemotaxis
         β€˜Find-me’ signals
         Attraction signals
         Danger signals
         DAMPs
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-010-0472-1/MediaObjects/10495_2010_472_Fig3_HTML.gif
      isPartOf:
         name:Apoptosis
         issn:
            1573-675X
            1360-8185
         volumeNumber:15
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Christoph Peter
            affiliation:
                  name:University of Tuebingen
                  address:
                     name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Sebastian Wesselborg
            affiliation:
                  name:University of Tuebingen
                  address:
                     name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Martin Herrmann
            affiliation:
                  name:University Hospital Erlangen
                  address:
                     name:Institute for Clinical Immunology, Department for Internal Medicine 3, University Hospital Erlangen, Erlangen, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kirsten Lauber
            affiliation:
                  name:University of Tuebingen
                  address:
                     name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
                     type:PostalAddress
                  type:Organization
                  name:Eberhard-Karls-University
                  address:
                     name:Department of Internal Medicine I, Eberhard-Karls-University, Tuebingen, Germany
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Apoptosis
      issn:
         1573-675X
         1360-8185
      volumeNumber:15
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Tuebingen
      address:
         name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
         type:PostalAddress
      name:University of Tuebingen
      address:
         name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
         type:PostalAddress
      name:University Hospital Erlangen
      address:
         name:Institute for Clinical Immunology, Department for Internal Medicine 3, University Hospital Erlangen, Erlangen, Germany
         type:PostalAddress
      name:University of Tuebingen
      address:
         name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
         type:PostalAddress
      name:Eberhard-Karls-University
      address:
         name:Department of Internal Medicine I, Eberhard-Karls-University, Tuebingen, Germany
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Christoph Peter
      affiliation:
            name:University of Tuebingen
            address:
               name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
               type:PostalAddress
            type:Organization
      name:Sebastian Wesselborg
      affiliation:
            name:University of Tuebingen
            address:
               name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
               type:PostalAddress
            type:Organization
      name:Martin Herrmann
      affiliation:
            name:University Hospital Erlangen
            address:
               name:Institute for Clinical Immunology, Department for Internal Medicine 3, University Hospital Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
      name:Kirsten Lauber
      affiliation:
            name:University of Tuebingen
            address:
               name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
               type:PostalAddress
            type:Organization
            name:Eberhard-Karls-University
            address:
               name:Department of Internal Medicine I, Eberhard-Karls-University, Tuebingen, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
      name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
      name:Institute for Clinical Immunology, Department for Internal Medicine 3, University Hospital Erlangen, Erlangen, Germany
      name:Section of Molecular Gastroenterology, Department of Internal Medicine I, University of Tuebingen, Tuebingen, Germany
      name:Department of Internal Medicine I, Eberhard-Karls-University, Tuebingen, Germany
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {πŸ”—}(614)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Prism.js

CDN Services {πŸ“¦}

  • Crossref

5.44s.