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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
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00281-013-0384-6.

Title:
Molecular mechanisms regulating NETosis in infection and disease | Seminars in Immunopathology
Description:
Neutrophils are the foot soldiers of the immune system. They home in to the site of infection and kill pathogens by phagocytosis, degranulation, and the release of web-like structures called neutrophil extracellular traps (NETs) that trap and kill a variety of microbes. NETs have been shown to play a multitude of additional roles in immunity but have also been implicated in inflammatory and autoimmune disease. Here, we discuss the role of NETs in these various contexts with a particular emphasis on the molecular mechanisms that regulate NET release and clearance. We highlight the comprehensive concepts and explore the important open questions in the field.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {๐Ÿ“š}

  • Science
  • Telecommunications
  • Education

Content Management System {๐Ÿ“}

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 {๐Ÿ“ˆ}

What is the average monthly size of link.springer.com audience?

๐ŸŒ  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? {๐Ÿ’ธ}

We find it hard to spot revenue streams.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {๐Ÿ”}

nets, net, google, scholar, neutrophil, neutrophils, pubmed, cas, formation, release, extracellular, netosis, infection, patients, cells, traps, role, cell, killing, disease, induce, important, mice, immune, antimicrobial, systemic, immunol, shown, chromatin, activation, infections, human, mpo, activity, ros, studies, proteins, defense, form, lupus, mechanisms, microbes, response, fungal, pad, sle, protein, mechanism, cgd, deficient,

Topics {โœ’๏ธ}

human immunodeficiency virus human immunodeficiency virus-1 neutrophil elastase-mediated degradation bayer-technicon automated hematology deep vein thrombosis mouse mrl/ltr model coli-induced netosis stems transforming growth factor-ฮฒ systemic lupus erythematosus anti-histone antibodies abrogate cell death-mediated pathway chronic granulomatous disease cell-activating factor baff anti-pad4 neutralizing antibodies beta-hydroxybutyrate abrogates formation foeโ€”netting neutrophils immobilize gram-negative bacterial pneumonia neutrophil-mediated platelet activation raf-mek-erk pathway neutrophil-specific protease escapes anti-neutrophil cytoplasmic antibodies plasmodium falciparum-infected children net-mediated thrombus formation guimaraes-costa ab tgf-ฮฒ inhibition resulted impairing thrombomodulin-dependent protein article download pdf pinto-da-silva lh dnase i-deficient mice wild-type mouse serum mpo-deficient individuals illustrates netosis-mediated cell death short-ranged antimicrobial proteins human blood-derived neutrophils completely mpo-deficient individuals myeloid-related protein-14 contributes cell-helper neutrophils stimulate completely mpo-deficient patients von kockritz-blickwede tnf-ฮฑ-induced nets low-density granulocyte subset von willebrand factor feline leukemia virus inhibiting tgf-ฮฒ leads pore-forming virulence factors major antimicrobial phagocytes important anti-inflammatory strategy venizelos papayannopoulos reduced lesion size neutrophil extracellular traps

Questions {โ“}

  • Do NETs kill?
  • Gupta A, Hasler P, Gebhardt S, Holzgreve W, Hahn S (2006) Occurrence of neutrophil extracellular DNA traps (NETs) in pre-eclampsia: a link with elevated levels of cell-free DNA?
  • Gupta AK, Hasler P, Holzgreve W, Hahn S (2007) Neutrophil NETs: a novel contributor to preeclampsia-associated placental hypoxia?
  • Menegazzi R, Decleva E, Dri P (2012) Killing by neutrophil extracellular traps: fact or folklore?
  • Urban CF, Lourido S, Zychlinsky A (2006) How do microbes evade neutrophil killing?

Schema {๐Ÿ—บ๏ธ}

WebPage:
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         headline:Molecular mechanisms regulating NETosis in infection and disease
         description:Neutrophils are the foot soldiers of the immune system. They home in to the site of infection and kill pathogens by phagocytosis, degranulation, and the release of web-like structures called neutrophil extracellular traps (NETs) that trap and kill a variety of microbes. NETs have been shown to play a multitude of additional roles in immunity but have also been implicated in inflammatory and autoimmune disease. Here, we discuss the role of NETs in these various contexts with a particular emphasis on the molecular mechanisms that regulate NET release and clearance. We highlight the comprehensive concepts and explore the important open questions in the field.
         datePublished:2013-06-04T00:00:00Z
         dateModified:2013-06-04T00:00:00Z
         pageStart:513
         pageEnd:530
         sameAs:https://doi.org/10.1007/s00281-013-0384-6
         keywords:
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            Systemic Lupus Erythematosus
            Systemic Lupus Erythematosus Patient
            Chronic Granulomatous Disease
            Neutrophil Elastase
            Immunology
            Internal Medicine
            Pathology
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      headline:Molecular mechanisms regulating NETosis in infection and disease
      description:Neutrophils are the foot soldiers of the immune system. They home in to the site of infection and kill pathogens by phagocytosis, degranulation, and the release of web-like structures called neutrophil extracellular traps (NETs) that trap and kill a variety of microbes. NETs have been shown to play a multitude of additional roles in immunity but have also been implicated in inflammatory and autoimmune disease. Here, we discuss the role of NETs in these various contexts with a particular emphasis on the molecular mechanisms that regulate NET release and clearance. We highlight the comprehensive concepts and explore the important open questions in the field.
      datePublished:2013-06-04T00:00:00Z
      dateModified:2013-06-04T00:00:00Z
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         Human Immunodeficiency Virus
         Systemic Lupus Erythematosus
         Systemic Lupus Erythematosus Patient
         Chronic Granulomatous Disease
         Neutrophil Elastase
         Immunology
         Internal Medicine
         Pathology
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                  name:Medical Research Council National Institute for Medical Research
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               name:Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, London, UK
               type:PostalAddress
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      name:Venizelos Papayannopoulos
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               name:Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, London, UK
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      name:Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, London, UK

External Links {๐Ÿ”—}(359)

Analytics and Tracking {๐Ÿ“Š}

  • Google Tag Manager

Libraries {๐Ÿ“š}

  • Clipboard.js
  • Particles.js
  • Prism.js

CDN Services {๐Ÿ“ฆ}

  • Crossref

5.58s.