We are analyzing https://link.springer.com/article/10.1186/ar586.

Title:
Complement and systemic lupus erythematosus | Arthritis Research & Therapy
Description:
Complement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Complement proteins are deposited in inflamed tissues and, in experimental models, inhibition of C5 ameliorates disease in a murine model. As a further twist to the associations between the complement system and SLE, autoantibodies to some complement proteins, especially to C1q, develop as part of the autoantibody response. The presence of anti-C1q autoantibodies is associated with severe illness, including glomerulonephritis. In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Health & Fitness
Education

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? {💸}

We don't see any clear sign of profit-making.

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 has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

complement, pubmed, google, scholar, cas, sle, lupus, patients, immune, erythematosus, systemic, deficiency, complexes, activation, disease, autoantibodies, immunol, levels, cells, central, proteins, pathway, med, complex, role, receptor, classical, walport, exp, clin, protein, rheum, injury, evidence, arthritis, activity, mice, erythrocytes, development, inflammatory, cell, clinical, response, anticq, antibodies, apoptotic, presence, glomerulonephritis, binding, autoantigens,

Topics {✒️}

enzyme-linked immunosorbent assay l'absorption du facteur erythrocyte-immune complex-glomerulonephritis connection anti-c1q autoantibody-negative patients late-acting complement components immune-complex-mediated pathology reverse-passive arthus reaction c1q solid-phase radioimmunoassay t-cell-dependent antigens [161] similar anti-c5 antibodies hypocomplementaemic urticarial vasculitis anti-c1q antibodies fix anti-c1q antibodies arise classical pathway-mediated hypocomplementemia continual low-level activation anti-c1 inhibitor autoantibodies remove anti-c1q autoantibodies membrane-targeted complement inhibitors arthritis research campaign immune-complex-mediated injury privacy choices/manage cookies autoantibody-mediated acquired deficiency immune-complex-mediated glomerulonephritis springer semin immunopathol immune-complex-mediated inflammation complement cascade plasma proteins β2-glycoprotein anti-c5 therapy anti-c1q antibody levels phospholipid-binding protein complexes complement genetically-deficient mice fresh frozen plasma defective immune-adherence solid phase assays fc–fc interactions sle-specific cutaneous lesions systemic lupus erythematosus c1-esterase inhibitor curr opin neurol wener mh trinder pk solid phase c1q undergoing experimental evaluation autoimmune haemolytic anaemia article number s279 fc receptor type lupus erythematosus globulin acute phase reactants ahearn jm primary antiphospholipid syndrome

Questions {❓}

Esdaile JM, Joseph L, Abrahamowicz M, Li Y, Danoff D, Clarke AE: Routine immunologic tests in systemic lupus erythematosus: is there a need for more studies?
How do these data explain how on the one hand C1q deficiency causes SLE and on the other that SLE causes an autoantibody response to C1q?
How is complement activated in SLE?
Swaak AJ, Smeenk RJ: Following the disease course in systemic lupus erythematosus: are serologic variables of any use?
What is the explanation for these clinical findings?
What is the source of these autoantigens?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Complement and systemic lupus erythematosus
         description:Complement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Complement proteins are deposited in inflamed tissues and, in experimental models, inhibition of C5 ameliorates disease in a murine model. As a further twist to the associations between the complement system and SLE, autoantibodies to some complement proteins, especially to C1q, develop as part of the autoantibody response. The presence of anti-C1q autoantibodies is associated with severe illness, including glomerulonephritis. In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus.
         datePublished:2002-05-09T00:00:00Z
         dateModified:2002-05-09T00:00:00Z
         pageStart:1
         pageEnd:15
         sameAs:https://doi.org/10.1186/ar586
         keywords:
            C1q
            complement
            glomerulonephritis
            lupus
            SLE
            Rheumatology
            Orthopedics
         image:
         isPartOf:
            name:Arthritis Research & Therapy
            issn:
               1478-6362
            volumeNumber:4
            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:Mark J Walport
               affiliation:
                     name:Imperial College of Science, Technology and Medicine
                     address:
                        name:Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Complement and systemic lupus erythematosus
      description:Complement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Complement proteins are deposited in inflamed tissues and, in experimental models, inhibition of C5 ameliorates disease in a murine model. As a further twist to the associations between the complement system and SLE, autoantibodies to some complement proteins, especially to C1q, develop as part of the autoantibody response. The presence of anti-C1q autoantibodies is associated with severe illness, including glomerulonephritis. In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus.
      datePublished:2002-05-09T00:00:00Z
      dateModified:2002-05-09T00:00:00Z
      pageStart:1
      pageEnd:15
      sameAs:https://doi.org/10.1186/ar586
      keywords:
         C1q
         complement
         glomerulonephritis
         lupus
         SLE
         Rheumatology
         Orthopedics
      image:
      isPartOf:
         name:Arthritis Research & Therapy
         issn:
            1478-6362
         volumeNumber:4
         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:Mark J Walport
            affiliation:
                  name:Imperial College of Science, Technology and Medicine
                  address:
                     name:Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Arthritis Research & Therapy
      issn:
         1478-6362
      volumeNumber:4
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Imperial College of Science, Technology and Medicine
      address:
         name:Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Mark J Walport
      affiliation:
            name:Imperial College of Science, Technology and Medicine
            address:
               name:Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK

External Links {🔗}(423)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.62s.

LINK . SPRINGER . COM {}