Genetic sharing and heritability of paediatric age of onset autoimmune diseases

Autoimmune diseases (AIDs) are polygenic diseases affecting 7–10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations...

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Published inNature communications Vol. 6; no. 1; p. 8442
Main Authors Li, Yun R., Zhao, Sihai D., Li, Jin, Bradfield, Jonathan P., Mohebnasab, Maede, Steel, Laura, Kobie, Julie, Abrams, Debra J., Mentch, Frank D., Glessner, Joseph T., Guo, Yiran, Wei, Zhi, Connolly, John J., Cardinale, Christopher J., Bakay, Marina, Li, Dong, Maggadottir, S. Melkorka, Thomas, Kelly A., Qui, Haijun, Chiavacci, Rosetta M., Kim, Cecilia E., Wang, Fengxiang, Snyder, James, Flatø, Berit, Førre, Øystein, Denson, Lee A., Thompson, Susan D., Becker, Mara L., Guthery, Stephen L., Latiano, Anna, Perez, Elena, Resnick, Elena, Strisciuglio, Caterina, Staiano, Annamaria, Miele, Erasmo, Silverberg, Mark S., Lie, Benedicte A., Punaro, Marilynn, Russell, Richard K., Wilson, David C., Dubinsky, Marla C., Monos, Dimitri S., Annese, Vito, Munro, Jane E., Wise, Carol, Chapel, Helen, Cunningham-Rundles, Charlotte, Orange, Jordan S., Behrens, Edward M., Sullivan, Kathleen E., Kugathasan, Subra, Griffiths, Anne M., Satsangi, Jack, Grant, Struan F. A., Sleiman, Patrick M. A., Finkel, Terri H., Polychronakos, Constantin, Baldassano, Robert N., Luning Prak, Eline T., Ellis, Justine A., Li, Hongzhe, Keating, Brendan J., Hakonarson, Hakon
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.10.2015
Nature Publishing Group
Nature Pub. Group
Subjects
38/39
631/208/2489/144
692/699/249/1313
692/700/1720
Adolescent
Age of Onset
Autoimmune diseases
Autoimmune Diseases - congenital
Autoimmune Diseases - genetics
Case-Control Studies
Child
Child, Preschool
Female
Genetic Predisposition to Disease
Genome-Wide Association Study
Humanities and Social Sciences
Humans
Male
multidisciplinary
Polymorphism, Single Nucleotide
Risk sharing
Science
Science (multidisciplinary)
White People - genetics
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/ncomms9442

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Abstract Autoimmune diseases (AIDs) are polygenic diseases affecting 7–10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP -h 2 ). SNP- h 2 estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP -h 2 in T1D and JIA, but does not significantly contribute to the pairwise rG . Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts. Autoimmune diseases are genetically complex disorders that affect up to 10% of the Western population. Here Li et al . quantify the heritability of a range of autoimmune diseases in the largest paediatric cohort examined to date, illustrating that genetic and non-genetic components variably contribute to the susceptibility of each disease.
AbstractList Autoimmune diseases (AIDs) are polygenic diseases affecting 7–10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP -h 2 ). SNP- h 2 estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP -h 2 in T1D and JIA, but does not significantly contribute to the pairwise rG . Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts. Autoimmune diseases are genetically complex disorders that affect up to 10% of the Western population. Here Li et al . quantify the heritability of a range of autoimmune diseases in the largest paediatric cohort examined to date, illustrating that genetic and non-genetic components variably contribute to the susceptibility of each disease.
Autoimmune diseases (AIDs) are polygenic diseases affecting 7-10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP-h2 ). SNP-h2 estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP-h2 in T1D and JIA, but does not significantly contribute to the pairwise rG. Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts.
Autoimmune diseases (AIDs) are polygenic diseases affecting 7-10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP-h(2)). SNP-h(2) estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP-h(2) in T1D and JIA, but does not significantly contribute to the pairwise rG. Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts.Autoimmune diseases (AIDs) are polygenic diseases affecting 7-10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP-h(2)). SNP-h(2) estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP-h(2) in T1D and JIA, but does not significantly contribute to the pairwise rG. Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts.
Autoimmune diseases (AIDs) are polygenic diseases affecting 7–10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP -h 2 ). SNP- h 2 estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP -h 2 in T1D and JIA, but does not significantly contribute to the pairwise rG . Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts.
Autoimmune diseases (AIDs) are polygenic diseases affecting 7-10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify the heritability of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to common genomic variations (SNP-h(2)). SNP-h(2) estimates are most significant for T1D (0.863±s.e. 0.07) and JIA (0.727±s.e. 0.037), more modest for UC (0.386±s.e. 0.04) and CD (0.454±0.025), largely consistent with population estimates and are generally greater than that previously reported by adult GWAS. On pairwise analysis, we observed that the diseases UC-CD (0.69±s.e. 0.07) and JIA-CVID (0.343±s.e. 0.13) are the most strongly correlated. Variations across the MHC strongly contribute to SNP-h(2) in T1D and JIA, but does not significantly contribute to the pairwise rG. Together, our results partition contributions of shared versus disease-specific genomic variations to pAID heritability, identifying pAIDs with unexpected risk sharing, while recapitulating known associations between autoimmune diseases previously reported in adult cohorts.
ArticleNumber 8442
Author Flatø, Berit
Silverberg, Mark S.
Ellis, Justine A.
Li, Yun R.
Strisciuglio, Caterina
Wei, Zhi
Connolly, John J.
Steel, Laura
Snyder, James
Kim, Cecilia E.
Cunningham-Rundles, Charlotte
Cardinale, Christopher J.
Wang, Fengxiang
Keating, Brendan J.
Baldassano, Robert N.
Satsangi, Jack
Zhao, Sihai D.
Chiavacci, Rosetta M.
Russell, Richard K.
Mentch, Frank D.
Orange, Jordan S.
Wise, Carol
Finkel, Terri H.
Bakay, Marina
Li, Hongzhe
Dubinsky, Marla C.
Bradfield, Jonathan P.
Li, Dong
Guo, Yiran
Punaro, Marilynn
Kobie, Julie
Behrens, Edward M.
Maggadottir, S. Melkorka
Sleiman, Patrick M. A.
Thomas, Kelly A.
Kugathasan, Subra
Hakonarson, Hakon
Polychronakos, Constantin
Resnick, Elena
Glessner, Joseph T.
Sullivan, Kathleen E.
Lie, Benedicte A.
Monos, Dimitri S.
Becker, Mara L.
Thompson, Susan D.
Miele, Erasmo
Griffiths, Anne M.
Perez, Elena
Grant, Struan F. A.
Staiano, Annamaria
Abrams, Debra J.
Denson, Lee A.
Munro, Jane E.
Førre, Øystein
Qui, Haijun
Annese, Vito
Mohebnasab, Maede
Wilson, David C.
Chapel, Helen
Luning Prak, Eline T.
Li, Jin
Latiano, Anna
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26450413$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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Snippet Autoimmune diseases (AIDs) are polygenic diseases affecting 7–10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify...
Autoimmune diseases (AIDs) are polygenic diseases affecting 7-10% of the population in the Western Hemisphere with few effective therapies. Here, we quantify...
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StartPage 8442
SubjectTerms 38/39
631/208/2489/144
692/699/249/1313
692/700/1720
Adolescent
Age of Onset
Autoimmune diseases
Autoimmune Diseases - congenital
Autoimmune Diseases - genetics
Case-Control Studies
Child
Child, Preschool
Female
Genetic Predisposition to Disease
Genome-Wide Association Study
Humanities and Social Sciences
Humans
Male
multidisciplinary
Polymorphism, Single Nucleotide
Risk sharing
Science
Science (multidisciplinary)
White People - genetics
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Title Genetic sharing and heritability of paediatric age of onset autoimmune diseases
URI https://link.springer.com/article/10.1038/ncomms9442
https://www.ncbi.nlm.nih.gov/pubmed/26450413
https://www.proquest.com/docview/1720453845
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https://pubmed.ncbi.nlm.nih.gov/PMC4633631
Volume 6
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