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We began analyzing https://www.nature.com/articles/ng.583, but it redirected us to https://www.nature.com/articles/ng.583. The analysis below is for the second page.

Title[redir]:
A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility | Nature Genetics
Description:
Yuta Kochi and colleagues identify a regulatory variant in CCR6 associated with susceptibility to rheumatoid arthritis. CCR6 encodes a chemokine receptor expressed on a subset of helper T cells known as Th17 cells, suggesting a possible role for CCR6 in Th17-driven autoimmunity. Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here, through a genome-wide association study of rheumatoid arthritis, we identified a polymorphism in CCR6, the gene encoding chemokine (C-C motif) receptor 6 (a surface marker for Th17 cells) at 6q27, that was associated with rheumatoid arthritis susceptibility and was validated in two independent replication cohorts from Japan (rs3093024, a total of 7,069 individuals with rheumatoid arthritis (cases) and 20,727 controls, overall odds ratio = 1.19, P = 7.7 × 10−19). We identified a triallelic dinucleotide polymorphism of CCR6 (CCR6DNP) in strong linkage disequilibrium with rs3093024 that showed effects on gene transcription. The CCR6DNP genotype was correlated with the expression level of CCR6 and was associated with the presence of interleukin-17 (IL-17) in the sera of subjects with rheumatoid arthritis. Moreover, CCR6DNP was associated with susceptibility to Graves

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

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While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

arthritis, rheumatoid, google, scholar, nature, genet, association, japan, nat, ccr, cells, study, access, data, article, susceptibility, disease, genomewide, risk, japanese, population, laboratory, analyzed, content, analysis, genetics, diseases, med, riken, tokyo, cookies, kochi, okada, yamamoto, autoimmune, gene, chemokine, functional, studies, university, research, medicine, cgm, yokohama, privacy, suzuki, genetic, polymorphism, encoding, replication,

Topics {✒️}

nature portfolio permissions reprints privacy policy ifn-gamma-producing γδ effector advertising allied research basic research tnf-α-stimulated thp-1 cells nature 423 nature 447 nature 449 nature genome-wide association studies social media genotyping development genome-wide association defines genetic-based association studies genome-wide association study population-based association studies author correspondence springerlink instant access nf-κb family nonsynonymous single-nucleotide polymorphism population-based linkage analyses permissions ccr6-expressing th17 cells european economic area biobank japan project human genome center fourth control cohort privacy rheumatoid arthritis association th17 cells predominate competing financial interests article kochi human th17 cells complex genetic etiology incorporating genetic networks single nucleotide polymorphism strong linkage disequilibrium common autoimmune disease explore content subscription content joint autoimmune inflammation germinal center-related rheumatoid arthritis networking institutional subscriptions read ccr5 mark subsets systemic lupus erythematosus il12/il23 pathway

Questions {❓}

  • Crohn's disease: Th1, Th17 or both?

Schema {🗺️}

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         headline:A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility
         description:Yuta Kochi and colleagues identify a regulatory variant in CCR6 associated with susceptibility to rheumatoid arthritis. CCR6 encodes a chemokine receptor expressed on a subset of helper T cells known as Th17 cells, suggesting a possible role for CCR6 in Th17-driven autoimmunity. Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here, through a genome-wide association study of rheumatoid arthritis, we identified a polymorphism in CCR6, the gene encoding chemokine (C-C motif) receptor 6 (a surface marker for Th17 cells) at 6q27, that was associated with rheumatoid arthritis susceptibility and was validated in two independent replication cohorts from Japan (rs3093024, a total of 7,069 individuals with rheumatoid arthritis (cases) and 20,727 controls, overall odds ratio = 1.19, P = 7.7 × 10−19). We identified a triallelic dinucleotide polymorphism of CCR6 (CCR6DNP) in strong linkage disequilibrium with rs3093024 that showed effects on gene transcription. The CCR6DNP genotype was correlated with the expression level of CCR6 and was associated with the presence of interleukin-17 (IL-17) in the sera of subjects with rheumatoid arthritis. Moreover, CCR6DNP was associated with susceptibility to Graves' and Crohn's diseases. These results suggest that CCR6 is critically involved in IL-17–driven autoimmunity in human diseases.
         datePublished:2010-05-09T00:00:00Z
         dateModified:2010-05-09T00:00:00Z
         pageStart:515
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            Genome-wide association studies
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            Human Genetics
            Cancer Research
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      headline:A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility
      description:Yuta Kochi and colleagues identify a regulatory variant in CCR6 associated with susceptibility to rheumatoid arthritis. CCR6 encodes a chemokine receptor expressed on a subset of helper T cells known as Th17 cells, suggesting a possible role for CCR6 in Th17-driven autoimmunity. Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here, through a genome-wide association study of rheumatoid arthritis, we identified a polymorphism in CCR6, the gene encoding chemokine (C-C motif) receptor 6 (a surface marker for Th17 cells) at 6q27, that was associated with rheumatoid arthritis susceptibility and was validated in two independent replication cohorts from Japan (rs3093024, a total of 7,069 individuals with rheumatoid arthritis (cases) and 20,727 controls, overall odds ratio = 1.19, P = 7.7 × 10−19). We identified a triallelic dinucleotide polymorphism of CCR6 (CCR6DNP) in strong linkage disequilibrium with rs3093024 that showed effects on gene transcription. The CCR6DNP genotype was correlated with the expression level of CCR6 and was associated with the presence of interleukin-17 (IL-17) in the sera of subjects with rheumatoid arthritis. Moreover, CCR6DNP was associated with susceptibility to Graves' and Crohn's diseases. These results suggest that CCR6 is critically involved in IL-17–driven autoimmunity in human diseases.
      datePublished:2010-05-09T00:00:00Z
      dateModified:2010-05-09T00:00:00Z
      pageStart:515
      pageEnd:519
      sameAs:https://doi.org/10.1038/ng.583
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         Gene regulation
         Genetic predisposition to disease
         Genome-wide association studies
         Rheumatoid arthritis
         Biomedicine
         general
         Human Genetics
         Cancer Research
         Agriculture
         Gene Function
         Animal Genetics and Genomics
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fng.583/MediaObjects/41588_2010_Article_BFng583_Fig1_HTML.jpg
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      author:
            name:Yuta Kochi
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      name:Nature Genetics
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      volumeNumber:42
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