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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/s11892-020-01318-8.

Title:
Early Onset of Autoimmune Diabetes in Children with Down Syndrome—Two Separate Aetiologies or an Immune System Pre-Programmed for Autoimmunity? | Current Diabetes Reports
Description:
Purpose of Review An increased frequency of autoimmunity in children with Down syndrome (DS) is well described but few studies have investigated the underlying mechanisms. Recent immune system investigation of individuals with DS may shed light on the increased risk of autoimmune conditions including type 1 diabetes. Recent Findings Diagnosis of type 1 diabetes is accelerated in children with DS with 17% diagnosed at, or under, the age of 2 years compared with only 4% in the same age group in the general population. Counterintuitively, children with DS and diabetes have less human leukocyte antigen (HLA)-mediated susceptibility than age-matched children with autoimmune diabetes from the general population. Early onset of diabetes in DS is further highlighted by the recent description of neonatal cases of diabetes which is autoimmune but not HLA associated. There are two potential explanations for this accelerated onset: (1) an additional chromosome 21 increases the genetic and immunological risk of autoimmune diabetes or (2) there are two separate aetiologies in children with DS and diabetes. Summary Autoimmunity in DS is an under-investigated area. In this review, we will draw on recent mechanistic studies in individuals with DS which shed some light on the increased risk of autoimmunity in children with DS and consider the current support for and against two aetiologies underlying diabetes in children with DS.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • Science

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

We're unsure if the website is profiting.

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 be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

diabetes, pubmed, children, syndrome, google, scholar, type, autoimmunity, cas, study, autoimmune, increased, central, risk, downs, studies, cells, early, immune, islet, population, individuals, age, hla, chromosome, cell, article, frequency, compared, general, disease, clinical, autoantibodies, genet, years, decreased, interferon, expression, mellitus, data, onset, recent, life, genes, showed, ubasha, med, analysis, system, underlying,

Topics {✒️}

highest-risk genotype dr4-dq8/dr3-dq2 immune system pre-programmed extra-thyroidal autoimmune disorders genome-wide association studies open access published t-lymphocyte subset imbalance current diabetes reports nationwide population-based study high-risk hla haplotypes impaired cell-mediated immunity mass cytometry approaches genotype-phenotype correlations age-matched control subjects article download pdf diabetes-specific tyrosine phosphatase identify genomic regions complications search search decreased hla-mediated susceptibility late-onset islet autoimmunity natural gene-expression variation recent population-based study early-onset diabetes mellitus kinase reciprocally regulates privacy choices/manage cookies hamilton-shield jp age-matched control population sex-matched healthy controls high-resolution mapping bmc med genet van der vossen strategies based global thymic hypofunction autoimmune thyroid diseases t-reg suppression [54••] protein tyrosine phosphorylation de weerd na underlying autoimmune environment arch environ health regulates ectopic expression european economic area basal ifn signalling animal subjects performed cell type-specific human leukocyte antigen current support t-lymphocyte subsets questionnaire-based study demonstrates early onset conditions privacy policy full access

Questions {❓}

  • Early Onset of Autoimmune Diabetes in Children with Down Syndrome—Two Separate Aetiologies or an Immune System Pre-Programmed for Autoimmunity?
  • Early Onset of Autoimmune Diabetes in Children with Down Syndrome—Two Separate Aetiologies or an Immune System Pre-Programmed for Autoimmunity?
  • How frequent is coeliac disease in Down syndrome?
  • Immune dysfunction in down's syndrome: primary immune deficiency or early senescence of the immune system?
  • Is disomic homozygosity at the APECED locus the cause of increased autoimmunity in Down's syndrome?
  • What factors influence recruitment to a birth cohort of infants with Down's syndrome?
  • Why do children with DS and diabetes have less HLA risk?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Early Onset of Autoimmune Diabetes in Children with Down Syndrome—Two Separate Aetiologies or an Immune System Pre-Programmed for Autoimmunity?
         description:An increased frequency of autoimmunity in children with Down syndrome (DS) is well described but few studies have investigated the underlying mechanisms. Recent immune system investigation of individuals with DS may shed light on the increased risk of autoimmune conditions including type 1 diabetes. Diagnosis of type 1 diabetes is accelerated in children with DS with 17% diagnosed at, or under, the age of 2 years compared with only 4% in the same age group in the general population. Counterintuitively, children with DS and diabetes have less human leukocyte antigen (HLA)-mediated susceptibility than age-matched children with autoimmune diabetes from the general population. Early onset of diabetes in DS is further highlighted by the recent description of neonatal cases of diabetes which is autoimmune but not HLA associated. There are two potential explanations for this accelerated onset: (1) an additional chromosome 21 increases the genetic and immunological risk of autoimmune diabetes or (2) there are two separate aetiologies in children with DS and diabetes. Autoimmunity in DS is an under-investigated area. In this review, we will draw on recent mechanistic studies in individuals with DS which shed some light on the increased risk of autoimmunity in children with DS and consider the current support for and against two aetiologies underlying diabetes in children with DS.
         datePublished:2020-08-25T00:00:00Z
         dateModified:2020-08-25T00:00:00Z
         pageStart:1
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         keywords:
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            Type 1 diabetes (T1D)
            Autoimmunity
            Islet autoantibodies
            HLA
            Diabetes
         image:
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         isPartOf:
            name:Current Diabetes Reports
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               name:Georgina L. Mortimer
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                        name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
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               name:Kathleen M. Gillespie
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ScholarlyArticle:
      headline:Early Onset of Autoimmune Diabetes in Children with Down Syndrome—Two Separate Aetiologies or an Immune System Pre-Programmed for Autoimmunity?
      description:An increased frequency of autoimmunity in children with Down syndrome (DS) is well described but few studies have investigated the underlying mechanisms. Recent immune system investigation of individuals with DS may shed light on the increased risk of autoimmune conditions including type 1 diabetes. Diagnosis of type 1 diabetes is accelerated in children with DS with 17% diagnosed at, or under, the age of 2 years compared with only 4% in the same age group in the general population. Counterintuitively, children with DS and diabetes have less human leukocyte antigen (HLA)-mediated susceptibility than age-matched children with autoimmune diabetes from the general population. Early onset of diabetes in DS is further highlighted by the recent description of neonatal cases of diabetes which is autoimmune but not HLA associated. There are two potential explanations for this accelerated onset: (1) an additional chromosome 21 increases the genetic and immunological risk of autoimmune diabetes or (2) there are two separate aetiologies in children with DS and diabetes. Autoimmunity in DS is an under-investigated area. In this review, we will draw on recent mechanistic studies in individuals with DS which shed some light on the increased risk of autoimmunity in children with DS and consider the current support for and against two aetiologies underlying diabetes in children with DS.
      datePublished:2020-08-25T00:00:00Z
      dateModified:2020-08-25T00:00:00Z
      pageStart:1
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      license:http://creativecommons.org/licenses/by/4.0/
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         Down syndrome
         Type 1 diabetes (T1D)
         Autoimmunity
         Islet autoantibodies
         HLA
         Diabetes
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11892-020-01318-8/MediaObjects/11892_2020_1318_Fig1_HTML.png
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      author:
            name:Georgina L. Mortimer
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                  name:University of Bristol
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                     name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kathleen M. Gillespie
            affiliation:
                  name:University of Bristol
                  address:
                     name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
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      name:Georgina L. Mortimer
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               name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
               type:PostalAddress
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      name:Kathleen M. Gillespie
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            name:University of Bristol
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               name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
               type:PostalAddress
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PostalAddress:
      name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK
      name:Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, Southmead Hospital, University of Bristol, Bristol, UK

External Links {🔗}(164)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.47s.