The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide
Objective The HLA shared epitope (SE) alleles are primarily a risk factor for the presence of antibodies to cyclic citrullinated peptide (anti‐CCP antibodies) rather than for the development of rheumatoid arthritis (RA). The SE alleles interact with the environmental risk factor tobacco exposure (TE...
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| Veröffentlicht in: | Arthritis and rheumatism 2007-02, Vol.56 (2), p.425-432 |
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| creator | van der Helm‐van Mil, Annette H. M. Verpoort, Kirsten N. le Cessie, Saskia Huizinga, Tom W. J. de Vries, René R. P. Toes, René E. M. |
| description | Objective
The HLA shared epitope (SE) alleles are primarily a risk factor for the presence of antibodies to cyclic citrullinated peptide (anti‐CCP antibodies) rather than for the development of rheumatoid arthritis (RA). The SE alleles interact with the environmental risk factor tobacco exposure (TE) for predisposition to anti‐CCP+ RA. The objectives of this study were to determine 1) whether different SE subtypes contribute differently to the presence of anti‐CCP antibodies, 2) whether different SE subtypes all interact with TE for the development of anti‐CCP antibodies, and 3) the effect of TE in relation to the SE alleles and anti‐CCP antibodies on the risk of progression from undifferentiated arthritis (UA) to RA.
Methods
We assessed the effect of SE subtypes and TE on the presence and level of anti‐CCP antibodies and on the risk of progression from UA to RA in 977 patients with early arthritis who were included in the Leiden Early Arthritis Clinic.
Results
The HLA–DRB1*0401, *0404, *0405, or *0408 SE alleles conferred the highest risk of developing anti‐CCP antibodies (odds ratio [OR] 5.0, compared with an OR of 2.0 for the HLA–DRB1*0101 or *0102 SE alleles and an OR of 1.7 for the HLA–DRB1*1001 SE allele). Conversely, the TE–SE allele interaction was the strongest for the HLA–DRB1*0101 or *0102 SE alleles and the HLA–DRB1*1001 SE allele. TE in SE+, anti‐CCP+ patients correlated with higher levels of anti‐CCP antibodies and with progression from UA to RA. In logistic regression analysis, only the presence and level of anti‐CCP antibodies were associated independently with RA development.
Conclusion
The HLA–DRB1 SE subtypes differ in their interaction with smoking and in their predisposition to anti‐CCP antibodies. TE contributes to the development of RA in SE+, anti‐CCP+ patients, which is explained by its effect on the level of anti‐CCP antibodies. |
| doi_str_mv | 10.1002/art.22373 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69038430</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20301460</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3843-ac83be15680ccc30c9dcd7730b23f51205970d7ef0782599577c52692685101d3</originalsourceid><addsrcrecordid>eNqF0c9uEzEQBnALgWgoHHgB5AtIHLYd2_F695iWP0WKhFSF88qxZ8mAs7vYjqrceAFOvCFPgtNE6glxssb-eb7Dx9hLARcCQF7amC-kVEY9YjOhZVuBUOIxmwHAvFK6FWfsWUrfyiiVVk_ZmTCy1nNjZuzXaoP8Zrn48_P3u9srwdPGRvQcJ8rjhNyGgAET99T3GDkNPBdPQ8ZoXaZx4HeUNzxtx-80fOV28Hwq_ylNY6L79zyW20zr0VPZUya3d4Ecd5TjLgQabC55E06ZPD5nT3obEr44nefsy4f3q-ubavn546frxbJyqpmryrpGrVHougHnnALXeueNUbCWqtdCgm4NeIM9mEbqttXGOC3rVtaNFiC8OmdvjnunOP7YYcrdlpLDEOyA4y51dQuHIPgvlKBAzOsDfHuELo4pRey7KdLWxn0noDuU1JWSuvuSin11Wrpbb9E_yFMrBbw-AZucDX20g6P04Bottarr4i6P7o4C7v-d2C1uV8fovwGUqew</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20301460</pqid></control><display><type>article</type><title>The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>van der Helm‐van Mil, Annette H. M. ; Verpoort, Kirsten N. ; le Cessie, Saskia ; Huizinga, Tom W. J. ; de Vries, René R. P. ; Toes, René E. M.</creator><creatorcontrib>van der Helm‐van Mil, Annette H. M. ; Verpoort, Kirsten N. ; le Cessie, Saskia ; Huizinga, Tom W. J. ; de Vries, René R. P. ; Toes, René E. M.</creatorcontrib><description>Objective
The HLA shared epitope (SE) alleles are primarily a risk factor for the presence of antibodies to cyclic citrullinated peptide (anti‐CCP antibodies) rather than for the development of rheumatoid arthritis (RA). The SE alleles interact with the environmental risk factor tobacco exposure (TE) for predisposition to anti‐CCP+ RA. The objectives of this study were to determine 1) whether different SE subtypes contribute differently to the presence of anti‐CCP antibodies, 2) whether different SE subtypes all interact with TE for the development of anti‐CCP antibodies, and 3) the effect of TE in relation to the SE alleles and anti‐CCP antibodies on the risk of progression from undifferentiated arthritis (UA) to RA.
Methods
We assessed the effect of SE subtypes and TE on the presence and level of anti‐CCP antibodies and on the risk of progression from UA to RA in 977 patients with early arthritis who were included in the Leiden Early Arthritis Clinic.
Results
The HLA–DRB1*0401, *0404, *0405, or *0408 SE alleles conferred the highest risk of developing anti‐CCP antibodies (odds ratio [OR] 5.0, compared with an OR of 2.0 for the HLA–DRB1*0101 or *0102 SE alleles and an OR of 1.7 for the HLA–DRB1*1001 SE allele). Conversely, the TE–SE allele interaction was the strongest for the HLA–DRB1*0101 or *0102 SE alleles and the HLA–DRB1*1001 SE allele. TE in SE+, anti‐CCP+ patients correlated with higher levels of anti‐CCP antibodies and with progression from UA to RA. In logistic regression analysis, only the presence and level of anti‐CCP antibodies were associated independently with RA development.
Conclusion
The HLA–DRB1 SE subtypes differ in their interaction with smoking and in their predisposition to anti‐CCP antibodies. TE contributes to the development of RA in SE+, anti‐CCP+ patients, which is explained by its effect on the level of anti‐CCP antibodies.</description><identifier>ISSN: 0004-3591</identifier><identifier>EISSN: 1529-0131</identifier><identifier>DOI: 10.1002/art.22373</identifier><identifier>PMID: 17265477</identifier><identifier>CODEN: ARHEAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Alleles ; Antibodies - immunology ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - physiopathology ; Biological and medical sciences ; Cohort Studies ; Disease Progression ; Epitopes - genetics ; Epitopes - immunology ; Female ; Genetic Predisposition to Disease ; HLA-DR Antigens - genetics ; HLA-DR Antigens - immunology ; HLA-DRB1 Chains ; Humans ; Male ; Medical sciences ; Middle Aged ; Peptides, Cyclic - immunology ; Peptides, Cyclic - physiology ; Protein Binding ; Risk Factors ; Smoking - genetics ; Smoking - immunology ; Tobacco Products ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Arthritis and rheumatism, 2007-02, Vol.56 (2), p.425-432</ispartof><rights>Copyright © 2007 by the American College of Rheumatology</rights><rights>2007 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3843-ac83be15680ccc30c9dcd7730b23f51205970d7ef0782599577c52692685101d3</citedby><cites>FETCH-LOGICAL-c3843-ac83be15680ccc30c9dcd7730b23f51205970d7ef0782599577c52692685101d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fart.22373$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.22373$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18525366$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17265477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Helm‐van Mil, Annette H. M.</creatorcontrib><creatorcontrib>Verpoort, Kirsten N.</creatorcontrib><creatorcontrib>le Cessie, Saskia</creatorcontrib><creatorcontrib>Huizinga, Tom W. J.</creatorcontrib><creatorcontrib>de Vries, René R. P.</creatorcontrib><creatorcontrib>Toes, René E. M.</creatorcontrib><title>The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide</title><title>Arthritis and rheumatism</title><addtitle>Arthritis Rheum</addtitle><description>Objective
The HLA shared epitope (SE) alleles are primarily a risk factor for the presence of antibodies to cyclic citrullinated peptide (anti‐CCP antibodies) rather than for the development of rheumatoid arthritis (RA). The SE alleles interact with the environmental risk factor tobacco exposure (TE) for predisposition to anti‐CCP+ RA. The objectives of this study were to determine 1) whether different SE subtypes contribute differently to the presence of anti‐CCP antibodies, 2) whether different SE subtypes all interact with TE for the development of anti‐CCP antibodies, and 3) the effect of TE in relation to the SE alleles and anti‐CCP antibodies on the risk of progression from undifferentiated arthritis (UA) to RA.
Methods
We assessed the effect of SE subtypes and TE on the presence and level of anti‐CCP antibodies and on the risk of progression from UA to RA in 977 patients with early arthritis who were included in the Leiden Early Arthritis Clinic.
Results
The HLA–DRB1*0401, *0404, *0405, or *0408 SE alleles conferred the highest risk of developing anti‐CCP antibodies (odds ratio [OR] 5.0, compared with an OR of 2.0 for the HLA–DRB1*0101 or *0102 SE alleles and an OR of 1.7 for the HLA–DRB1*1001 SE allele). Conversely, the TE–SE allele interaction was the strongest for the HLA–DRB1*0101 or *0102 SE alleles and the HLA–DRB1*1001 SE allele. TE in SE+, anti‐CCP+ patients correlated with higher levels of anti‐CCP antibodies and with progression from UA to RA. In logistic regression analysis, only the presence and level of anti‐CCP antibodies were associated independently with RA development.
Conclusion
The HLA–DRB1 SE subtypes differ in their interaction with smoking and in their predisposition to anti‐CCP antibodies. TE contributes to the development of RA in SE+, anti‐CCP+ patients, which is explained by its effect on the level of anti‐CCP antibodies.</description><subject>Adult</subject><subject>Aged</subject><subject>Alleles</subject><subject>Antibodies - immunology</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Cohort Studies</subject><subject>Disease Progression</subject><subject>Epitopes - genetics</subject><subject>Epitopes - immunology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>HLA-DR Antigens - genetics</subject><subject>HLA-DR Antigens - immunology</subject><subject>HLA-DRB1 Chains</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Peptides, Cyclic - immunology</subject><subject>Peptides, Cyclic - physiology</subject><subject>Protein Binding</subject><subject>Risk Factors</subject><subject>Smoking - genetics</subject><subject>Smoking - immunology</subject><subject>Tobacco Products</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>0004-3591</issn><issn>1529-0131</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c9uEzEQBnALgWgoHHgB5AtIHLYd2_F695iWP0WKhFSF88qxZ8mAs7vYjqrceAFOvCFPgtNE6glxssb-eb7Dx9hLARcCQF7amC-kVEY9YjOhZVuBUOIxmwHAvFK6FWfsWUrfyiiVVk_ZmTCy1nNjZuzXaoP8Zrn48_P3u9srwdPGRvQcJ8rjhNyGgAET99T3GDkNPBdPQ8ZoXaZx4HeUNzxtx-80fOV28Hwq_ylNY6L79zyW20zr0VPZUya3d4Ecd5TjLgQabC55E06ZPD5nT3obEr44nefsy4f3q-ubavn546frxbJyqpmryrpGrVHougHnnALXeueNUbCWqtdCgm4NeIM9mEbqttXGOC3rVtaNFiC8OmdvjnunOP7YYcrdlpLDEOyA4y51dQuHIPgvlKBAzOsDfHuELo4pRey7KdLWxn0noDuU1JWSuvuSin11Wrpbb9E_yFMrBbw-AZucDX20g6P04Bottarr4i6P7o4C7v-d2C1uV8fovwGUqew</recordid><startdate>200702</startdate><enddate>200702</enddate><creator>van der Helm‐van Mil, Annette H. M.</creator><creator>Verpoort, Kirsten N.</creator><creator>le Cessie, Saskia</creator><creator>Huizinga, Tom W. J.</creator><creator>de Vries, René R. P.</creator><creator>Toes, René E. M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>IQODW</scope><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>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200702</creationdate><title>The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide</title><author>van der Helm‐van Mil, Annette H. M. ; Verpoort, Kirsten N. ; le Cessie, Saskia ; Huizinga, Tom W. J. ; de Vries, René R. P. ; Toes, René E. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3843-ac83be15680ccc30c9dcd7730b23f51205970d7ef0782599577c52692685101d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Alleles</topic><topic>Antibodies - immunology</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Cohort Studies</topic><topic>Disease Progression</topic><topic>Epitopes - genetics</topic><topic>Epitopes - immunology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>HLA-DR Antigens - genetics</topic><topic>HLA-DR Antigens - immunology</topic><topic>HLA-DRB1 Chains</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Peptides, Cyclic - immunology</topic><topic>Peptides, Cyclic - physiology</topic><topic>Protein Binding</topic><topic>Risk Factors</topic><topic>Smoking - genetics</topic><topic>Smoking - immunology</topic><topic>Tobacco Products</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>online_resources</toplevel><creatorcontrib>van der Helm‐van Mil, Annette H. M.</creatorcontrib><creatorcontrib>Verpoort, Kirsten N.</creatorcontrib><creatorcontrib>le Cessie, Saskia</creatorcontrib><creatorcontrib>Huizinga, Tom W. J.</creatorcontrib><creatorcontrib>de Vries, René R. P.</creatorcontrib><creatorcontrib>Toes, René E. M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis and rheumatism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Helm‐van Mil, Annette H. M.</au><au>Verpoort, Kirsten N.</au><au>le Cessie, Saskia</au><au>Huizinga, Tom W. J.</au><au>de Vries, René R. P.</au><au>Toes, René E. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide</atitle><jtitle>Arthritis and rheumatism</jtitle><addtitle>Arthritis Rheum</addtitle><date>2007-02</date><risdate>2007</risdate><volume>56</volume><issue>2</issue><spage>425</spage><epage>432</epage><pages>425-432</pages><issn>0004-3591</issn><eissn>1529-0131</eissn><coden>ARHEAW</coden><abstract>Objective
The HLA shared epitope (SE) alleles are primarily a risk factor for the presence of antibodies to cyclic citrullinated peptide (anti‐CCP antibodies) rather than for the development of rheumatoid arthritis (RA). The SE alleles interact with the environmental risk factor tobacco exposure (TE) for predisposition to anti‐CCP+ RA. The objectives of this study were to determine 1) whether different SE subtypes contribute differently to the presence of anti‐CCP antibodies, 2) whether different SE subtypes all interact with TE for the development of anti‐CCP antibodies, and 3) the effect of TE in relation to the SE alleles and anti‐CCP antibodies on the risk of progression from undifferentiated arthritis (UA) to RA.
Methods
We assessed the effect of SE subtypes and TE on the presence and level of anti‐CCP antibodies and on the risk of progression from UA to RA in 977 patients with early arthritis who were included in the Leiden Early Arthritis Clinic.
Results
The HLA–DRB1*0401, *0404, *0405, or *0408 SE alleles conferred the highest risk of developing anti‐CCP antibodies (odds ratio [OR] 5.0, compared with an OR of 2.0 for the HLA–DRB1*0101 or *0102 SE alleles and an OR of 1.7 for the HLA–DRB1*1001 SE allele). Conversely, the TE–SE allele interaction was the strongest for the HLA–DRB1*0101 or *0102 SE alleles and the HLA–DRB1*1001 SE allele. TE in SE+, anti‐CCP+ patients correlated with higher levels of anti‐CCP antibodies and with progression from UA to RA. In logistic regression analysis, only the presence and level of anti‐CCP antibodies were associated independently with RA development.
Conclusion
The HLA–DRB1 SE subtypes differ in their interaction with smoking and in their predisposition to anti‐CCP antibodies. TE contributes to the development of RA in SE+, anti‐CCP+ patients, which is explained by its effect on the level of anti‐CCP antibodies.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17265477</pmid><doi>10.1002/art.22373</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Aged Alleles Antibodies - immunology Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - physiopathology Biological and medical sciences Cohort Studies Disease Progression Epitopes - genetics Epitopes - immunology Female Genetic Predisposition to Disease HLA-DR Antigens - genetics HLA-DR Antigens - immunology HLA-DRB1 Chains Humans Male Medical sciences Middle Aged Peptides, Cyclic - immunology Peptides, Cyclic - physiology Protein Binding Risk Factors Smoking - genetics Smoking - immunology Tobacco Products Tobacco, tobacco smoking Toxicology |
| title | The HLA–DRB1 shared epitope alleles differ in the interaction with smoking and predisposition to antibodies to cyclic citrullinated peptide |
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