A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides

Introduction. Rheumatoid arthritis (RA) patients can be classified based on presence or absence of anticitrullinated peptide antibodies (ACPA) in their serum. This heterogeneity among patients may reflect important biological differences underlying the disease process. To date, the majority of genet...

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Autores: Bossini Castillo, Lara, Kovel, C. de, Kallberg, H., Slot, R. van 't, Italiaander, A., Coenen, M., Tak, P. P., Posthumus, M. D., Wijmenga, Cisca, Huizinga, Tom, Helm-van Mil, A. H. M. van der, Stoeken-Rijsbergen, G., Rodríguez-Rodríguez, Luis, Balsa, Alejandro, González Álvaro, Isidoro, González-Gay, Miguel A., Gómez Vaquero, Carmen, Franke, B., LifeLines Cohort Study, Vermeulen, S., Horst-Bruinsma, I. E. van der, Dijkmans, B. A. C., Wolbink, G. J., Ophoff, Roel A., Maehlen, M. T., Riel, P. van, Merriman, M., Klareskog, L., Lie, Benedicte A., Merriman, Tony, Crusius, J. B. A., Brouwer, E., Martín, Javier, Vries, N. de, Toes, R., Padyukov, Leonid, Koeleman, Bobby P. C.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2015
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/113070
Acceso en línea:https://hdl.handle.net/2445/113070
Access Level:acceso abierto
Palabra clave:Artritis reumatoide
Genomes
Genòmica
Anticossos monoclonals
Pèptids
Rheumatoid arthritis
Genomics
Monoclonal antibodies
Peptides
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spelling A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptidesBossini Castillo, LaraKovel, C. deKallberg, H.Slot, R. van 'tItaliaander, A.Coenen, M.Tak, P. P.Posthumus, M. D.Wijmenga, CiscaHuizinga, TomHelm-van Mil, A. H. M. van derStoeken-Rijsbergen, G.Rodríguez-Rodríguez, LuisBalsa, AlejandroGonzález Álvaro, IsidoroGonzález-Gay, Miguel A.Gómez Vaquero, CarmenFranke, B.LifeLines Cohort StudyVermeulen, S.Horst-Bruinsma, I. E. van derDijkmans, B. A. C.Wolbink, G. J.Ophoff, Roel A.Maehlen, M. T.Riel, P. vanMerriman, M.Klareskog, L.Lie, Benedicte A.Merriman, TonyCrusius, J. B. A.Brouwer, E.Martín, JavierVries, N. deToes, R.Padyukov, LeonidKoeleman, Bobby P. C.Artritis reumatoideGenomesGenòmicaAnticossos monoclonalsPèptidsRheumatoid arthritisGenomesGenomicsMonoclonal antibodiesPeptidesIntroduction. Rheumatoid arthritis (RA) patients can be classified based on presence or absence of anticitrullinated peptide antibodies (ACPA) in their serum. This heterogeneity among patients may reflect important biological differences underlying the disease process. To date, the majority of genetic studies have focused on the ACPA-positive group. Therefore, our goal was to analyse the genetic risk factors that contribute to ACPA-negative RA. Methods. We performed a large-scale genome-wide association study (GWAS) in three Caucasian European cohorts comprising 1148 ACPA-negative RA patients and 6008 controls. All patients were screened using the Illumina Human Cyto-12 chip, and controls were genotyped using different genome-wide platforms. Population-independent analyses were carried out by means of logistic regression. Meta-analysis with previously published data was performed as follow-up for selected signals (reaching a total of 1922 ACPA-negative RA patients and 7087 controls). Imputation of classical HLA alleles, aminoacid residues and single nucleotide polymorphisms was undertaken. Results. The combined analysis of the studied cohorts resulted in identification of a peak of association in the HLA-region and several suggestive non-HLA associations. Meta-analysis with previous reports confirmed the association of the HLA region with this subset and an observed association in the CLYBL locus remained suggestive. The imputation and deep interrogation of the HLA region led to identification of a two aminoacid model (HLA-B at position 9 and HLA-DRB1 at position 11) that accounted for the observed genome-wide associations in this region. Conclusions. Our study shed light on the influence of the HLA region in ACPA-negative RA and identified a suggestive risk locus for this condition.BMJ Publishing Group2015info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/113070Articles publicats en revistes (Ciències Clíniques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.1136/annrheumdis-2013-204591Annals of the Rheumatic Diseases, 2015, vol. 74, num. 3, p. e15https://doi.org/10.1136/annrheumdis-2013-204591(c) BMJ Publishing Group, 2015info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1130702026-05-27T06:46:51Z
dc.title.none.fl_str_mv A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
title A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
spellingShingle A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
Bossini Castillo, Lara
Artritis reumatoide
Genomes
Genòmica
Anticossos monoclonals
Pèptids
Rheumatoid arthritis
Genomes
Genomics
Monoclonal antibodies
Peptides
title_short A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
title_full A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
title_fullStr A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
title_full_unstemmed A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
title_sort A genome-wide association study of rheumatoid arthritis without antibodies against citrullinated peptides
dc.creator.none.fl_str_mv Bossini Castillo, Lara
Kovel, C. de
Kallberg, H.
Slot, R. van 't
Italiaander, A.
Coenen, M.
Tak, P. P.
Posthumus, M. D.
Wijmenga, Cisca
Huizinga, Tom
Helm-van Mil, A. H. M. van der
Stoeken-Rijsbergen, G.
Rodríguez-Rodríguez, Luis
Balsa, Alejandro
González Álvaro, Isidoro
González-Gay, Miguel A.
Gómez Vaquero, Carmen
Franke, B.
LifeLines Cohort Study
Vermeulen, S.
Horst-Bruinsma, I. E. van der
Dijkmans, B. A. C.
Wolbink, G. J.
Ophoff, Roel A.
Maehlen, M. T.
Riel, P. van
Merriman, M.
Klareskog, L.
Lie, Benedicte A.
Merriman, Tony
Crusius, J. B. A.
Brouwer, E.
Martín, Javier
Vries, N. de
Toes, R.
Padyukov, Leonid
Koeleman, Bobby P. C.
author Bossini Castillo, Lara
author_facet Bossini Castillo, Lara
Kovel, C. de
Kallberg, H.
Slot, R. van 't
Italiaander, A.
Coenen, M.
Tak, P. P.
Posthumus, M. D.
Wijmenga, Cisca
Huizinga, Tom
Helm-van Mil, A. H. M. van der
Stoeken-Rijsbergen, G.
Rodríguez-Rodríguez, Luis
Balsa, Alejandro
González Álvaro, Isidoro
González-Gay, Miguel A.
Gómez Vaquero, Carmen
Franke, B.
LifeLines Cohort Study
Vermeulen, S.
Horst-Bruinsma, I. E. van der
Dijkmans, B. A. C.
Wolbink, G. J.
Ophoff, Roel A.
Maehlen, M. T.
Riel, P. van
Merriman, M.
Klareskog, L.
Lie, Benedicte A.
Merriman, Tony
Crusius, J. B. A.
Brouwer, E.
Martín, Javier
Vries, N. de
Toes, R.
Padyukov, Leonid
Koeleman, Bobby P. C.
author_role author
author2 Kovel, C. de
Kallberg, H.
Slot, R. van 't
Italiaander, A.
Coenen, M.
Tak, P. P.
Posthumus, M. D.
Wijmenga, Cisca
Huizinga, Tom
Helm-van Mil, A. H. M. van der
Stoeken-Rijsbergen, G.
Rodríguez-Rodríguez, Luis
Balsa, Alejandro
González Álvaro, Isidoro
González-Gay, Miguel A.
Gómez Vaquero, Carmen
Franke, B.
LifeLines Cohort Study
Vermeulen, S.
Horst-Bruinsma, I. E. van der
Dijkmans, B. A. C.
Wolbink, G. J.
Ophoff, Roel A.
Maehlen, M. T.
Riel, P. van
Merriman, M.
Klareskog, L.
Lie, Benedicte A.
Merriman, Tony
Crusius, J. B. A.
Brouwer, E.
Martín, Javier
Vries, N. de
Toes, R.
Padyukov, Leonid
Koeleman, Bobby P. C.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Artritis reumatoide
Genomes
Genòmica
Anticossos monoclonals
Pèptids
Rheumatoid arthritis
Genomes
Genomics
Monoclonal antibodies
Peptides
topic Artritis reumatoide
Genomes
Genòmica
Anticossos monoclonals
Pèptids
Rheumatoid arthritis
Genomes
Genomics
Monoclonal antibodies
Peptides
description Introduction. Rheumatoid arthritis (RA) patients can be classified based on presence or absence of anticitrullinated peptide antibodies (ACPA) in their serum. This heterogeneity among patients may reflect important biological differences underlying the disease process. To date, the majority of genetic studies have focused on the ACPA-positive group. Therefore, our goal was to analyse the genetic risk factors that contribute to ACPA-negative RA. Methods. We performed a large-scale genome-wide association study (GWAS) in three Caucasian European cohorts comprising 1148 ACPA-negative RA patients and 6008 controls. All patients were screened using the Illumina Human Cyto-12 chip, and controls were genotyped using different genome-wide platforms. Population-independent analyses were carried out by means of logistic regression. Meta-analysis with previously published data was performed as follow-up for selected signals (reaching a total of 1922 ACPA-negative RA patients and 7087 controls). Imputation of classical HLA alleles, aminoacid residues and single nucleotide polymorphisms was undertaken. Results. The combined analysis of the studied cohorts resulted in identification of a peak of association in the HLA-region and several suggestive non-HLA associations. Meta-analysis with previous reports confirmed the association of the HLA region with this subset and an observed association in the CLYBL locus remained suggestive. The imputation and deep interrogation of the HLA region led to identification of a two aminoacid model (HLA-B at position 9 and HLA-DRB1 at position 11) that accounted for the observed genome-wide associations in this region. Conclusions. Our study shed light on the influence of the HLA region in ACPA-negative RA and identified a suggestive risk locus for this condition.
publishDate 2015
dc.date.none.fl_str_mv 2015
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/113070
url https://hdl.handle.net/2445/113070
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.1136/annrheumdis-2013-204591
Annals of the Rheumatic Diseases, 2015, vol. 74, num. 3, p. e15
https://doi.org/10.1136/annrheumdis-2013-204591
dc.rights.none.fl_str_mv (c) BMJ Publishing Group, 2015
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) BMJ Publishing Group, 2015
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv BMJ Publishing Group
publisher.none.fl_str_mv BMJ Publishing Group
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Clíniques)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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