Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.

Anti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target ref...

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Main Authors: Jing Cui, Eli A Stahl, Saedis Saevarsdottir, Corinne Miceli, Dorothee Diogo, Gosia Trynka, Towfique Raj, Maša Umiċeviċ Mirkov, Helena Canhao, Katsunori Ikari, Chikashi Terao, Yukinori Okada, Sara Wedrén, Johan Askling, Hisashi Yamanaka, Shigeki Momohara, Atsuo Taniguchi, Koichiro Ohmura, Fumihiko Matsuda, Tsuneyo Mimori, Namrata Gupta, Manik Kuchroo, Ann W Morgan, John D Isaacs, Anthony G Wilson, Kimme L Hyrich, Marieke Herenius, Marieke E Doorenspleet, Paul-Peter Tak, J Bart A Crusius, Irene E van der Horst-Bruinsma, Gert Jan Wolbink, Piet L C M van Riel, Mart van de Laar, Henk-Jan Guchelaar, Nancy A Shadick, Cornelia F Allaart, Tom W J Huizinga, Rene E M Toes, Robert P Kimberly, S Louis Bridges, Lindsey A Criswell, Larry W Moreland, João Eurico Fonseca, Niek de Vries, Barbara E Stranger, Philip L De Jager, Soumya Raychaudhuri, Michael E Weinblatt, Peter K Gregersen, Xavier Mariette, Anne Barton, Leonid Padyukov, Marieke J H Coenen, Elizabeth W Karlson, Robert M Plenge
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-03-01
Series:PLoS Genetics
Online Access:https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1003394&type=printable
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author Jing Cui
Eli A Stahl
Saedis Saevarsdottir
Corinne Miceli
Dorothee Diogo
Gosia Trynka
Towfique Raj
Maša Umiċeviċ Mirkov
Helena Canhao
Helena Canhao
Katsunori Ikari
Chikashi Terao
Yukinori Okada
Sara Wedrén
Johan Askling
Hisashi Yamanaka
Shigeki Momohara
Atsuo Taniguchi
Koichiro Ohmura
Fumihiko Matsuda
Tsuneyo Mimori
Namrata Gupta
Manik Kuchroo
Ann W Morgan
John D Isaacs
Anthony G Wilson
Kimme L Hyrich
Marieke Herenius
Marieke E Doorenspleet
Paul-Peter Tak
J Bart A Crusius
Irene E van der Horst-Bruinsma
Gert Jan Wolbink
Piet L C M van Riel
Mart van de Laar
Henk-Jan Guchelaar
Nancy A Shadick
Cornelia F Allaart
Tom W J Huizinga
Rene E M Toes
Robert P Kimberly
S Louis Bridges
Lindsey A Criswell
Larry W Moreland
João Eurico Fonseca
Niek de Vries
Barbara E Stranger
Philip L De Jager
Soumya Raychaudhuri
Michael E Weinblatt
Peter K Gregersen
Xavier Mariette
Anne Barton
Leonid Padyukov
Marieke J H Coenen
Elizabeth W Karlson
Robert M Plenge
author_facet Jing Cui
Eli A Stahl
Saedis Saevarsdottir
Corinne Miceli
Dorothee Diogo
Gosia Trynka
Towfique Raj
Maša Umiċeviċ Mirkov
Helena Canhao
Helena Canhao
Katsunori Ikari
Chikashi Terao
Yukinori Okada
Sara Wedrén
Johan Askling
Hisashi Yamanaka
Shigeki Momohara
Atsuo Taniguchi
Koichiro Ohmura
Fumihiko Matsuda
Tsuneyo Mimori
Namrata Gupta
Manik Kuchroo
Ann W Morgan
John D Isaacs
Anthony G Wilson
Kimme L Hyrich
Marieke Herenius
Marieke E Doorenspleet
Paul-Peter Tak
J Bart A Crusius
Irene E van der Horst-Bruinsma
Gert Jan Wolbink
Piet L C M van Riel
Mart van de Laar
Henk-Jan Guchelaar
Nancy A Shadick
Cornelia F Allaart
Tom W J Huizinga
Rene E M Toes
Robert P Kimberly
S Louis Bridges
Lindsey A Criswell
Larry W Moreland
João Eurico Fonseca
Niek de Vries
Barbara E Stranger
Philip L De Jager
Soumya Raychaudhuri
Michael E Weinblatt
Peter K Gregersen
Xavier Mariette
Anne Barton
Leonid Padyukov
Marieke J H Coenen
Elizabeth W Karlson
Robert M Plenge
author_sort Jing Cui
collection DOAJ
description Anti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target refractory cases. To understand the biological basis of response to anti-TNF therapy, we conducted a genome-wide association study (GWAS) meta-analysis of more than 2 million common variants in 2,706 RA patients from 13 different collections. Patients were treated with one of three anti-TNF medications: etanercept (n = 733), infliximab (n = 894), or adalimumab (n = 1,071). We identified a SNP (rs6427528) at the 1q23 locus that was associated with change in disease activity score (ΔDAS) in the etanercept subset of patients (P = 8 × 10(-8)), but not in the infliximab or adalimumab subsets (P>0.05). The SNP is predicted to disrupt transcription factor binding site motifs in the 3' UTR of an immune-related gene, CD84, and the allele associated with better response to etanercept was associated with higher CD84 gene expression in peripheral blood mononuclear cells (P = 1 × 10(-11) in 228 non-RA patients and P = 0.004 in 132 RA patients). Consistent with the genetic findings, higher CD84 gene expression correlated with lower cross-sectional DAS (P = 0.02, n = 210) and showed a non-significant trend for better ΔDAS in a subset of RA patients with gene expression data (n = 31, etanercept-treated). A small, multi-ethnic replication showed a non-significant trend towards an association among etanercept-treated RA patients of Portuguese ancestry (n = 139, P = 0.4), but no association among patients of Japanese ancestry (n = 151, P = 0.8). Our study demonstrates that an allele associated with response to etanercept therapy is also associated with CD84 gene expression, and further that CD84 expression correlates with disease activity. These findings support a model in which CD84 genotypes and/or expression may serve as a useful biomarker for response to etanercept treatment in RA patients of European ancestry.
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language English
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record_format Article
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spelling doaj-art-81c1f31b39334e34b1f84c06c37997b42025-08-20T03:26:39ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042013-03-0193e100339410.1371/journal.pgen.1003394Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.Jing CuiEli A StahlSaedis SaevarsdottirCorinne MiceliDorothee DiogoGosia TrynkaTowfique RajMaša Umiċeviċ MirkovHelena CanhaoHelena CanhaoKatsunori IkariChikashi TeraoYukinori OkadaSara WedrénJohan AsklingHisashi YamanakaShigeki MomoharaAtsuo TaniguchiKoichiro OhmuraFumihiko MatsudaTsuneyo MimoriNamrata GuptaManik KuchrooAnn W MorganJohn D IsaacsAnthony G WilsonKimme L HyrichMarieke HereniusMarieke E DoorenspleetPaul-Peter TakJ Bart A CrusiusIrene E van der Horst-BruinsmaGert Jan WolbinkPiet L C M van RielMart van de LaarHenk-Jan GuchelaarNancy A ShadickCornelia F AllaartTom W J HuizingaRene E M ToesRobert P KimberlyS Louis BridgesLindsey A CriswellLarry W MorelandJoão Eurico FonsecaNiek de VriesBarbara E StrangerPhilip L De JagerSoumya RaychaudhuriMichael E WeinblattPeter K GregersenXavier MarietteAnne BartonLeonid PadyukovMarieke J H CoenenElizabeth W KarlsonRobert M PlengeAnti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target refractory cases. To understand the biological basis of response to anti-TNF therapy, we conducted a genome-wide association study (GWAS) meta-analysis of more than 2 million common variants in 2,706 RA patients from 13 different collections. Patients were treated with one of three anti-TNF medications: etanercept (n = 733), infliximab (n = 894), or adalimumab (n = 1,071). We identified a SNP (rs6427528) at the 1q23 locus that was associated with change in disease activity score (ΔDAS) in the etanercept subset of patients (P = 8 × 10(-8)), but not in the infliximab or adalimumab subsets (P>0.05). The SNP is predicted to disrupt transcription factor binding site motifs in the 3' UTR of an immune-related gene, CD84, and the allele associated with better response to etanercept was associated with higher CD84 gene expression in peripheral blood mononuclear cells (P = 1 × 10(-11) in 228 non-RA patients and P = 0.004 in 132 RA patients). Consistent with the genetic findings, higher CD84 gene expression correlated with lower cross-sectional DAS (P = 0.02, n = 210) and showed a non-significant trend for better ΔDAS in a subset of RA patients with gene expression data (n = 31, etanercept-treated). A small, multi-ethnic replication showed a non-significant trend towards an association among etanercept-treated RA patients of Portuguese ancestry (n = 139, P = 0.4), but no association among patients of Japanese ancestry (n = 151, P = 0.8). Our study demonstrates that an allele associated with response to etanercept therapy is also associated with CD84 gene expression, and further that CD84 expression correlates with disease activity. These findings support a model in which CD84 genotypes and/or expression may serve as a useful biomarker for response to etanercept treatment in RA patients of European ancestry.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1003394&type=printable
spellingShingle Jing Cui
Eli A Stahl
Saedis Saevarsdottir
Corinne Miceli
Dorothee Diogo
Gosia Trynka
Towfique Raj
Maša Umiċeviċ Mirkov
Helena Canhao
Helena Canhao
Katsunori Ikari
Chikashi Terao
Yukinori Okada
Sara Wedrén
Johan Askling
Hisashi Yamanaka
Shigeki Momohara
Atsuo Taniguchi
Koichiro Ohmura
Fumihiko Matsuda
Tsuneyo Mimori
Namrata Gupta
Manik Kuchroo
Ann W Morgan
John D Isaacs
Anthony G Wilson
Kimme L Hyrich
Marieke Herenius
Marieke E Doorenspleet
Paul-Peter Tak
J Bart A Crusius
Irene E van der Horst-Bruinsma
Gert Jan Wolbink
Piet L C M van Riel
Mart van de Laar
Henk-Jan Guchelaar
Nancy A Shadick
Cornelia F Allaart
Tom W J Huizinga
Rene E M Toes
Robert P Kimberly
S Louis Bridges
Lindsey A Criswell
Larry W Moreland
João Eurico Fonseca
Niek de Vries
Barbara E Stranger
Philip L De Jager
Soumya Raychaudhuri
Michael E Weinblatt
Peter K Gregersen
Xavier Mariette
Anne Barton
Leonid Padyukov
Marieke J H Coenen
Elizabeth W Karlson
Robert M Plenge
Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
PLoS Genetics
title Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
title_full Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
title_fullStr Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
title_full_unstemmed Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
title_short Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis.
title_sort genome wide association study and gene expression analysis identifies cd84 as a predictor of response to etanercept therapy in rheumatoid arthritis
url https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1003394&type=printable
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