The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status
We have recently described the association between rheumatoid arthritis and a coding single-nucleotide polymorphism in the intracellular protein tyrosine phosphatase, PTPN22. The disease-associated polymorphism, 1858 C/T (rs2476601), encodes an amino-acid change (R620W) in one of four SH3 domain bin...
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| Veröffentlicht in: | Genes and immunity 2005-03, Vol.6 (2), p.129-133 |
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| creator | Lee, A T Li, W Liew, A Bombardier, C Weisman, M Massarotti, E M Kent, J Wolfe, F Begovich, A B Gregersen, P K |
| description | We have recently described the association between rheumatoid arthritis and a coding single-nucleotide polymorphism in the intracellular protein tyrosine phosphatase, PTPN22. The disease-associated polymorphism, 1858 C/T (rs2476601), encodes an amino-acid change (R620W) in one of four SH3 domain binding sites in the PTPN22 molecule. We have now extended our initial studies to address three questions: (1) Is the association with rheumatoid arthritis limited to rheumatoid factor (RF) positive disease? (2) Does homozygosity for PTPN22 R620W substantially increase disease susceptibility? (3) Is there an interaction between PTPN22 and the rheumatoid arthritis (RA)-associated HLA-DRB1 shared epitope alleles? A total of 1413 Caucasian rheumatoid arthritis patients and 1401 Caucasian controls were genotyped. The results support the view that PTPN22 was strongly and preferentially associated with RF positive disease (OR=1.75, 95% CI 1.46–2.10,
P
=1.3 × 10
−9
). The PTPN22 risk allele was not significantly associated with RF negative disease (OR=1.19, 95% CI 0.92–1.53,
P
=0.18), although a very weak association cannot be completely excluded. There was a strong dose effect on disease risk; two copies of the PTPN22 R620W allele more than doubles the risk for RF positive RA (OR=4.57, 95% CI 2.35–8.89). There was no evidence of a genetic association between PTPN22 and HLA susceptibility alleles. |
| doi_str_mv | 10.1038/sj.gene.6364159 |
| format | Article |
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P
=1.3 × 10
−9
). The PTPN22 risk allele was not significantly associated with RF negative disease (OR=1.19, 95% CI 0.92–1.53,
P
=0.18), although a very weak association cannot be completely excluded. There was a strong dose effect on disease risk; two copies of the PTPN22 R620W allele more than doubles the risk for RF positive RA (OR=4.57, 95% CI 2.35–8.89). There was no evidence of a genetic association between PTPN22 and HLA susceptibility alleles.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6364159</identifier><identifier>PMID: 15674368</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Alleles ; Arthritis, Rheumatoid - genetics ; Binding sites ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cohort Studies ; Control ; Drb1 protein ; Epitopes ; full-paper ; Gene Expression ; Gene Frequency - genetics ; Gene polymorphism ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Histocompatibility antigen HLA ; Histocompatibility antigens ; HLA histocompatibility antigens ; HLA-DR Antigens - genetics ; HLA-DRB1 Chains ; Human Genetics ; Humans ; Immunology ; Linkage Disequilibrium ; Physiological aspects ; Polymorphism ; Polymorphism, Single Nucleotide - genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 22 ; Protein Tyrosine Phosphatases - genetics ; Protein-tyrosine-phosphatase ; Rheumatic diseases ; Rheumatoid arthritis ; Rheumatoid factor ; Rheumatoid Factor - genetics ; Risk Factors ; Serology ; Single-nucleotide polymorphism ; White people</subject><ispartof>Genes and immunity, 2005-03, Vol.6 (2), p.129-133</ispartof><rights>Springer Nature Limited 2005</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c564t-9dd16f6af0d12ed1c70608dd0a6094bc82ad391f916e3a52e79832f2716540563</citedby><cites>FETCH-LOGICAL-c564t-9dd16f6af0d12ed1c70608dd0a6094bc82ad391f916e3a52e79832f2716540563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.gene.6364159$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6364159$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15674368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, A T</creatorcontrib><creatorcontrib>Li, W</creatorcontrib><creatorcontrib>Liew, A</creatorcontrib><creatorcontrib>Bombardier, C</creatorcontrib><creatorcontrib>Weisman, M</creatorcontrib><creatorcontrib>Massarotti, E M</creatorcontrib><creatorcontrib>Kent, J</creatorcontrib><creatorcontrib>Wolfe, F</creatorcontrib><creatorcontrib>Begovich, A B</creatorcontrib><creatorcontrib>Gregersen, P K</creatorcontrib><title>The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>We have recently described the association between rheumatoid arthritis and a coding single-nucleotide polymorphism in the intracellular protein tyrosine phosphatase, PTPN22. The disease-associated polymorphism, 1858 C/T (rs2476601), encodes an amino-acid change (R620W) in one of four SH3 domain binding sites in the PTPN22 molecule. We have now extended our initial studies to address three questions: (1) Is the association with rheumatoid arthritis limited to rheumatoid factor (RF) positive disease? (2) Does homozygosity for PTPN22 R620W substantially increase disease susceptibility? (3) Is there an interaction between PTPN22 and the rheumatoid arthritis (RA)-associated HLA-DRB1 shared epitope alleles? A total of 1413 Caucasian rheumatoid arthritis patients and 1401 Caucasian controls were genotyped. The results support the view that PTPN22 was strongly and preferentially associated with RF positive disease (OR=1.75, 95% CI 1.46–2.10,
P
=1.3 × 10
−9
). The PTPN22 risk allele was not significantly associated with RF negative disease (OR=1.19, 95% CI 0.92–1.53,
P
=0.18), although a very weak association cannot be completely excluded. There was a strong dose effect on disease risk; two copies of the PTPN22 R620W allele more than doubles the risk for RF positive RA (OR=4.57, 95% CI 2.35–8.89). There was no evidence of a genetic association between PTPN22 and HLA susceptibility alleles.</description><subject>Alleles</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Binding sites</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cohort Studies</subject><subject>Control</subject><subject>Drb1 protein</subject><subject>Epitopes</subject><subject>full-paper</subject><subject>Gene Expression</subject><subject>Gene Frequency - genetics</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility antigens</subject><subject>HLA histocompatibility antigens</subject><subject>HLA-DR Antigens - genetics</subject><subject>HLA-DRB1 Chains</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Linkage Disequilibrium</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 22</subject><subject>Protein Tyrosine Phosphatases - genetics</subject><subject>Protein-tyrosine-phosphatase</subject><subject>Rheumatic diseases</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatoid factor</subject><subject>Rheumatoid Factor - genetics</subject><subject>Risk Factors</subject><subject>Serology</subject><subject>Single-nucleotide polymorphism</subject><subject>White people</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFksFrFDEUxgdRbK2evUlQEDzMNsnMJJNjKa0tFC3bFY8hO3mzm2Un2eZl1N79w82yC2XFIjkkvPd7X_iSryjeMjphtGpPcTVZgIeJqETNGvWsOGa1FGVTS_p8exairFupjopXiCtKmWBCvSyOWCNkXYn2uPg9WwK5nd1-4ZxMBaffySasH4YQN0uHAzGIoXMmAZKfLi3J9DL30SX3A0hcwjiYFJwlJqZlzFUkzhNDbEAoLWzAW_CJDMZ7iGQ-JuJD2gld3ZyVdxcEk0kjvi5e9GaN8Ga_nxTfLi9m51flzdfP1-dnN2XXiDqVylomemF6ahkHyzpJBW2tpUZQVc-7lhtbKdYrJqAyDQep2or3XDLR1LQR1Unxcae7ieF-BEx6cNjBem08hBF1fhSp6qb6L8hkW9FWyQx--AtchTH6bELz_COSN4LxTL1_kmJt1pFMPUotzBq0831I0XTbe_UZa7niKpvM1OQfVF4WBtcFD73L9YOBTwcDmUnwKy3MiKiv76aH7OmO7WJAjNDrTXSDiQ-aUb3Nm8aV3uZN7_OWJ97tnY3zAewjvw9YBugOwNzyC4iP1p_S_ANGBd31</recordid><startdate>20050301</startdate><enddate>20050301</enddate><creator>Lee, A T</creator><creator>Li, W</creator><creator>Liew, A</creator><creator>Bombardier, C</creator><creator>Weisman, M</creator><creator>Massarotti, E M</creator><creator>Kent, J</creator><creator>Wolfe, F</creator><creator>Begovich, A B</creator><creator>Gregersen, P K</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050301</creationdate><title>The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status</title><author>Lee, A T ; Li, W ; Liew, A ; Bombardier, C ; Weisman, M ; Massarotti, E M ; Kent, J ; Wolfe, F ; Begovich, A B ; Gregersen, P K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-9dd16f6af0d12ed1c70608dd0a6094bc82ad391f916e3a52e79832f2716540563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Alleles</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Binding sites</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cohort Studies</topic><topic>Control</topic><topic>Drb1 protein</topic><topic>Epitopes</topic><topic>full-paper</topic><topic>Gene Expression</topic><topic>Gene Frequency - genetics</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genetic Predisposition to Disease</topic><topic>Histocompatibility antigen HLA</topic><topic>Histocompatibility antigens</topic><topic>HLA histocompatibility antigens</topic><topic>HLA-DR Antigens - genetics</topic><topic>HLA-DRB1 Chains</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Linkage Disequilibrium</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 22</topic><topic>Protein Tyrosine Phosphatases - genetics</topic><topic>Protein-tyrosine-phosphatase</topic><topic>Rheumatic diseases</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatoid factor</topic><topic>Rheumatoid Factor - genetics</topic><topic>Risk Factors</topic><topic>Serology</topic><topic>Single-nucleotide polymorphism</topic><topic>White people</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, A T</creatorcontrib><creatorcontrib>Li, W</creatorcontrib><creatorcontrib>Liew, A</creatorcontrib><creatorcontrib>Bombardier, C</creatorcontrib><creatorcontrib>Weisman, M</creatorcontrib><creatorcontrib>Massarotti, E M</creatorcontrib><creatorcontrib>Kent, J</creatorcontrib><creatorcontrib>Wolfe, F</creatorcontrib><creatorcontrib>Begovich, A B</creatorcontrib><creatorcontrib>Gregersen, P K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, A T</au><au>Li, W</au><au>Liew, A</au><au>Bombardier, C</au><au>Weisman, M</au><au>Massarotti, E M</au><au>Kent, J</au><au>Wolfe, F</au><au>Begovich, A B</au><au>Gregersen, P K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>6</volume><issue>2</issue><spage>129</spage><epage>133</epage><pages>129-133</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>We have recently described the association between rheumatoid arthritis and a coding single-nucleotide polymorphism in the intracellular protein tyrosine phosphatase, PTPN22. The disease-associated polymorphism, 1858 C/T (rs2476601), encodes an amino-acid change (R620W) in one of four SH3 domain binding sites in the PTPN22 molecule. We have now extended our initial studies to address three questions: (1) Is the association with rheumatoid arthritis limited to rheumatoid factor (RF) positive disease? (2) Does homozygosity for PTPN22 R620W substantially increase disease susceptibility? (3) Is there an interaction between PTPN22 and the rheumatoid arthritis (RA)-associated HLA-DRB1 shared epitope alleles? A total of 1413 Caucasian rheumatoid arthritis patients and 1401 Caucasian controls were genotyped. The results support the view that PTPN22 was strongly and preferentially associated with RF positive disease (OR=1.75, 95% CI 1.46–2.10,
P
=1.3 × 10
−9
). The PTPN22 risk allele was not significantly associated with RF negative disease (OR=1.19, 95% CI 0.92–1.53,
P
=0.18), although a very weak association cannot be completely excluded. There was a strong dose effect on disease risk; two copies of the PTPN22 R620W allele more than doubles the risk for RF positive RA (OR=4.57, 95% CI 2.35–8.89). There was no evidence of a genetic association between PTPN22 and HLA susceptibility alleles.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15674368</pmid><doi>10.1038/sj.gene.6364159</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Genes and immunity, 2005-03, Vol.6 (2), p.129-133 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature - Complete Springer Journals |
| subjects | Alleles Arthritis, Rheumatoid - genetics Binding sites Biomedical and Life Sciences Biomedicine Cancer Research Cohort Studies Control Drb1 protein Epitopes full-paper Gene Expression Gene Frequency - genetics Gene polymorphism Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Histocompatibility antigen HLA Histocompatibility antigens HLA histocompatibility antigens HLA-DR Antigens - genetics HLA-DRB1 Chains Human Genetics Humans Immunology Linkage Disequilibrium Physiological aspects Polymorphism Polymorphism, Single Nucleotide - genetics Protein Tyrosine Phosphatase, Non-Receptor Type 22 Protein Tyrosine Phosphatases - genetics Protein-tyrosine-phosphatase Rheumatic diseases Rheumatoid arthritis Rheumatoid factor Rheumatoid Factor - genetics Risk Factors Serology Single-nucleotide polymorphism White people |
| title | The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status |
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