The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens
Objective Recent data suggest that a gene–environment interaction between smoking and the HLA shared epitope alleles plays a role in shaping the autoimmune reaction to specific citrullinated antigens. This study was undertaken to determine the effects of HLA shared epitope alleles and tobacco exposu...
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| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2011-07, Vol.63 (7), p.1823-1832 |
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| creator | Willemze, Annemiek van der Woude, Diane Ghidey, Wendimagegn Levarht, E. W. Nivine Stoeken‐Rijsbergen, Gerrie Verduyn, Willem de Vries, René R. P. Houwing‐Duistermaat, Jeanine J. Huizinga, Tom W. J. Trouw, Leendert A. Toes, René E. M. |
| description | Objective
Recent data suggest that a gene–environment interaction between smoking and the HLA shared epitope alleles plays a role in shaping the autoimmune reaction to specific citrullinated antigens. This study was undertaken to determine the effects of HLA shared epitope alleles and tobacco exposure on the immune response against various citrullinated antigens. These associations were analyzed in the anti–citrullinated protein antibody (ACPA)–positive stratum to control for the possibility that the associations found are explained by the known interaction between HLA shared epitope alleles and tobacco exposure on ACPA status.
Methods
In 661 patients with rheumatoid arthritis, reactivity against several citrullinated antigens from vimentin, fibrinogen, enolase, and myelin basic protein was determined by enzyme‐linked immunosorbent assay. The effects of the HLA shared epitope alleles and tobacco exposure were assessed by logistic regression analysis. Biologic interaction was analyzed by investigating whether the effects of the risk factors combined exhibited departure from additivity.
Results
A significant interaction between tobacco exposure and HLA shared epitope alleles was found for the presence of ACPA as reported previously. When these interaction effects were studied for several ACPA “fine specificities,” significant interactions were noted for several citrullinated peptides. However, these interactions were not present after stratification for ACPA status, indicating that the interaction between tobacco exposure and HLA shared epitope alleles influences autoimmunity not to specific citrullinated antigens, but rather to ACPA development.
Conclusion
Our data indicate that the gene–environment interaction between HLA shared epitope alleles and smoking does not appear to shape the reactivity of the ACPA response. These data suggest that smoking promotes nonspecific citrullination rather than citrullination of specific antigens. |
| doi_str_mv | 10.1002/art.30409 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_874484467</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>874484467</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4159-c4a26c9780eef1985cc950f17782b2c1bc3772b306f425516b7f008c910e84e93</originalsourceid><addsrcrecordid>eNp90d2KEzEYBuAgitutHngDEhBZPehufieTw7KoKxQEqcdDJv2mmzWT1CTj0lvwqs22VUHQk_zAw_uRvAi9oOSSEsKuTCqXnAiiH6EZlUwvCOX0MZoRQsSCS03P0HnOd_XKuORP0RmjkjREqxn6sb4F7EKBZGxxMeAeyj1AwDerJc63JsEGw86VuANsvAcPGZuwwXmMX13YHs6uZGxjKMn10yGjRGymEt04TsGVPTZb40IuOMP3Osdj60qavHfBlBpvQnFbCPkZejIYn-H5aZ-jL-_fra9vFqtPHz5eL1cLK6jUdTWssVq1BGCgupXWakkGqlTLemZpb7lSrOekGQSTkja9GghpraYEWgGaz9HFMXeX4rcJculGly14bwLEKXetEqIVolFVvvmvpKIRQre6FZW--ovexSmF-o6OSqqIZqx-_hy9PSqbYs4Jhm6X3GjSvqOke6iyq1V2hyqrfXlKnPoRNr_lr-4qeH0CJlvjh2SCdfmPE1y2lD-4q6O7dx72_57YLT-vj6N_AoE9tdY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1517092202</pqid></control><display><type>article</type><title>The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Willemze, Annemiek ; van der Woude, Diane ; Ghidey, Wendimagegn ; Levarht, E. W. Nivine ; Stoeken‐Rijsbergen, Gerrie ; Verduyn, Willem ; de Vries, René R. P. ; Houwing‐Duistermaat, Jeanine J. ; Huizinga, Tom W. J. ; Trouw, Leendert A. ; Toes, René E. M.</creator><creatorcontrib>Willemze, Annemiek ; van der Woude, Diane ; Ghidey, Wendimagegn ; Levarht, E. W. Nivine ; Stoeken‐Rijsbergen, Gerrie ; Verduyn, Willem ; de Vries, René R. P. ; Houwing‐Duistermaat, Jeanine J. ; Huizinga, Tom W. J. ; Trouw, Leendert A. ; Toes, René E. M.</creatorcontrib><description>Objective
Recent data suggest that a gene–environment interaction between smoking and the HLA shared epitope alleles plays a role in shaping the autoimmune reaction to specific citrullinated antigens. This study was undertaken to determine the effects of HLA shared epitope alleles and tobacco exposure on the immune response against various citrullinated antigens. These associations were analyzed in the anti–citrullinated protein antibody (ACPA)–positive stratum to control for the possibility that the associations found are explained by the known interaction between HLA shared epitope alleles and tobacco exposure on ACPA status.
Methods
In 661 patients with rheumatoid arthritis, reactivity against several citrullinated antigens from vimentin, fibrinogen, enolase, and myelin basic protein was determined by enzyme‐linked immunosorbent assay. The effects of the HLA shared epitope alleles and tobacco exposure were assessed by logistic regression analysis. Biologic interaction was analyzed by investigating whether the effects of the risk factors combined exhibited departure from additivity.
Results
A significant interaction between tobacco exposure and HLA shared epitope alleles was found for the presence of ACPA as reported previously. When these interaction effects were studied for several ACPA “fine specificities,” significant interactions were noted for several citrullinated peptides. However, these interactions were not present after stratification for ACPA status, indicating that the interaction between tobacco exposure and HLA shared epitope alleles influences autoimmunity not to specific citrullinated antigens, but rather to ACPA development.
Conclusion
Our data indicate that the gene–environment interaction between HLA shared epitope alleles and smoking does not appear to shape the reactivity of the ACPA response. These data suggest that smoking promotes nonspecific citrullination rather than citrullination of specific antigens.</description><identifier>ISSN: 0004-3591</identifier><identifier>ISSN: 2326-5191</identifier><identifier>ISSN: 1529-0131</identifier><identifier>EISSN: 1529-0131</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.30409</identifier><identifier>PMID: 21506097</identifier><identifier>CODEN: ARHEAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Alleles ; Antibodies ; Antigens ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - immunology ; Autoantibodies - genetics ; Autoantibodies - immunology ; Autoimmunity - genetics ; Autoimmunity - immunology ; Biological and medical sciences ; Diseases of the osteoarticular system ; Enzyme-Linked Immunosorbent Assay ; Epitopes - genetics ; Epitopes - immunology ; Female ; Genetic Predisposition to Disease ; HLA Antigens - genetics ; HLA Antigens - immunology ; Humans ; Immune system ; Immunoglobulin M - genetics ; Immunoglobulin M - immunology ; Logistic Models ; Male ; Medical sciences ; Middle Aged ; Odds Ratio ; Risk Factors ; Smoking ; Smoking - genetics ; Smoking - immunology ; Tobacco ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2011-07, Vol.63 (7), p.1823-1832</ispartof><rights>Copyright © 2011 by the American College of Rheumatology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 by the American College of Rheumatology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4159-c4a26c9780eef1985cc950f17782b2c1bc3772b306f425516b7f008c910e84e93</citedby><cites>FETCH-LOGICAL-c4159-c4a26c9780eef1985cc950f17782b2c1bc3772b306f425516b7f008c910e84e93</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.30409$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.30409$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24358137$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21506097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Willemze, Annemiek</creatorcontrib><creatorcontrib>van der Woude, Diane</creatorcontrib><creatorcontrib>Ghidey, Wendimagegn</creatorcontrib><creatorcontrib>Levarht, E. W. Nivine</creatorcontrib><creatorcontrib>Stoeken‐Rijsbergen, Gerrie</creatorcontrib><creatorcontrib>Verduyn, Willem</creatorcontrib><creatorcontrib>de Vries, René R. P.</creatorcontrib><creatorcontrib>Houwing‐Duistermaat, Jeanine J.</creatorcontrib><creatorcontrib>Huizinga, Tom W. J.</creatorcontrib><creatorcontrib>Trouw, Leendert A.</creatorcontrib><creatorcontrib>Toes, René E. M.</creatorcontrib><title>The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheum</addtitle><description>Objective
Recent data suggest that a gene–environment interaction between smoking and the HLA shared epitope alleles plays a role in shaping the autoimmune reaction to specific citrullinated antigens. This study was undertaken to determine the effects of HLA shared epitope alleles and tobacco exposure on the immune response against various citrullinated antigens. These associations were analyzed in the anti–citrullinated protein antibody (ACPA)–positive stratum to control for the possibility that the associations found are explained by the known interaction between HLA shared epitope alleles and tobacco exposure on ACPA status.
Methods
In 661 patients with rheumatoid arthritis, reactivity against several citrullinated antigens from vimentin, fibrinogen, enolase, and myelin basic protein was determined by enzyme‐linked immunosorbent assay. The effects of the HLA shared epitope alleles and tobacco exposure were assessed by logistic regression analysis. Biologic interaction was analyzed by investigating whether the effects of the risk factors combined exhibited departure from additivity.
Results
A significant interaction between tobacco exposure and HLA shared epitope alleles was found for the presence of ACPA as reported previously. When these interaction effects were studied for several ACPA “fine specificities,” significant interactions were noted for several citrullinated peptides. However, these interactions were not present after stratification for ACPA status, indicating that the interaction between tobacco exposure and HLA shared epitope alleles influences autoimmunity not to specific citrullinated antigens, but rather to ACPA development.
Conclusion
Our data indicate that the gene–environment interaction between HLA shared epitope alleles and smoking does not appear to shape the reactivity of the ACPA response. These data suggest that smoking promotes nonspecific citrullination rather than citrullination of specific antigens.</description><subject>Adult</subject><subject>Aged</subject><subject>Alleles</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Autoantibodies - genetics</subject><subject>Autoantibodies - immunology</subject><subject>Autoimmunity - genetics</subject><subject>Autoimmunity - immunology</subject><subject>Biological and medical sciences</subject><subject>Diseases of the osteoarticular system</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Epitopes - genetics</subject><subject>Epitopes - immunology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>HLA Antigens - genetics</subject><subject>HLA Antigens - immunology</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunoglobulin M - genetics</subject><subject>Immunoglobulin M - immunology</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Risk Factors</subject><subject>Smoking</subject><subject>Smoking - genetics</subject><subject>Smoking - immunology</subject><subject>Tobacco</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>0004-3591</issn><issn>2326-5191</issn><issn>1529-0131</issn><issn>1529-0131</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90d2KEzEYBuAgitutHngDEhBZPehufieTw7KoKxQEqcdDJv2mmzWT1CTj0lvwqs22VUHQk_zAw_uRvAi9oOSSEsKuTCqXnAiiH6EZlUwvCOX0MZoRQsSCS03P0HnOd_XKuORP0RmjkjREqxn6sb4F7EKBZGxxMeAeyj1AwDerJc63JsEGw86VuANsvAcPGZuwwXmMX13YHs6uZGxjKMn10yGjRGymEt04TsGVPTZb40IuOMP3Osdj60qavHfBlBpvQnFbCPkZejIYn-H5aZ-jL-_fra9vFqtPHz5eL1cLK6jUdTWssVq1BGCgupXWakkGqlTLemZpb7lSrOekGQSTkja9GghpraYEWgGaz9HFMXeX4rcJculGly14bwLEKXetEqIVolFVvvmvpKIRQre6FZW--ovexSmF-o6OSqqIZqx-_hy9PSqbYs4Jhm6X3GjSvqOke6iyq1V2hyqrfXlKnPoRNr_lr-4qeH0CJlvjh2SCdfmPE1y2lD-4q6O7dx72_57YLT-vj6N_AoE9tdY</recordid><startdate>201107</startdate><enddate>201107</enddate><creator>Willemze, Annemiek</creator><creator>van der Woude, Diane</creator><creator>Ghidey, Wendimagegn</creator><creator>Levarht, E. W. Nivine</creator><creator>Stoeken‐Rijsbergen, Gerrie</creator><creator>Verduyn, Willem</creator><creator>de Vries, René R. P.</creator><creator>Houwing‐Duistermaat, Jeanine J.</creator><creator>Huizinga, Tom W. J.</creator><creator>Trouw, Leendert A.</creator><creator>Toes, René E. M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201107</creationdate><title>The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens</title><author>Willemze, Annemiek ; van der Woude, Diane ; Ghidey, Wendimagegn ; Levarht, E. W. Nivine ; Stoeken‐Rijsbergen, Gerrie ; Verduyn, Willem ; de Vries, René R. P. ; Houwing‐Duistermaat, Jeanine J. ; Huizinga, Tom W. J. ; Trouw, Leendert A. ; Toes, René E. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4159-c4a26c9780eef1985cc950f17782b2c1bc3772b306f425516b7f008c910e84e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Alleles</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Autoantibodies - genetics</topic><topic>Autoantibodies - immunology</topic><topic>Autoimmunity - genetics</topic><topic>Autoimmunity - immunology</topic><topic>Biological and medical sciences</topic><topic>Diseases of the osteoarticular system</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Epitopes - genetics</topic><topic>Epitopes - immunology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>HLA Antigens - genetics</topic><topic>HLA Antigens - immunology</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunoglobulin M - genetics</topic><topic>Immunoglobulin M - immunology</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Risk Factors</topic><topic>Smoking</topic><topic>Smoking - genetics</topic><topic>Smoking - immunology</topic><topic>Tobacco</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Willemze, Annemiek</creatorcontrib><creatorcontrib>van der Woude, Diane</creatorcontrib><creatorcontrib>Ghidey, Wendimagegn</creatorcontrib><creatorcontrib>Levarht, E. W. Nivine</creatorcontrib><creatorcontrib>Stoeken‐Rijsbergen, Gerrie</creatorcontrib><creatorcontrib>Verduyn, Willem</creatorcontrib><creatorcontrib>de Vries, René R. P.</creatorcontrib><creatorcontrib>Houwing‐Duistermaat, Jeanine J.</creatorcontrib><creatorcontrib>Huizinga, Tom W. J.</creatorcontrib><creatorcontrib>Trouw, Leendert A.</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Willemze, Annemiek</au><au>van der Woude, Diane</au><au>Ghidey, Wendimagegn</au><au>Levarht, E. W. Nivine</au><au>Stoeken‐Rijsbergen, Gerrie</au><au>Verduyn, Willem</au><au>de Vries, René R. P.</au><au>Houwing‐Duistermaat, Jeanine J.</au><au>Huizinga, Tom W. J.</au><au>Trouw, Leendert A.</au><au>Toes, René E. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheum</addtitle><date>2011-07</date><risdate>2011</risdate><volume>63</volume><issue>7</issue><spage>1823</spage><epage>1832</epage><pages>1823-1832</pages><issn>0004-3591</issn><issn>2326-5191</issn><issn>1529-0131</issn><eissn>1529-0131</eissn><eissn>2326-5205</eissn><coden>ARHEAW</coden><abstract>Objective
Recent data suggest that a gene–environment interaction between smoking and the HLA shared epitope alleles plays a role in shaping the autoimmune reaction to specific citrullinated antigens. This study was undertaken to determine the effects of HLA shared epitope alleles and tobacco exposure on the immune response against various citrullinated antigens. These associations were analyzed in the anti–citrullinated protein antibody (ACPA)–positive stratum to control for the possibility that the associations found are explained by the known interaction between HLA shared epitope alleles and tobacco exposure on ACPA status.
Methods
In 661 patients with rheumatoid arthritis, reactivity against several citrullinated antigens from vimentin, fibrinogen, enolase, and myelin basic protein was determined by enzyme‐linked immunosorbent assay. The effects of the HLA shared epitope alleles and tobacco exposure were assessed by logistic regression analysis. Biologic interaction was analyzed by investigating whether the effects of the risk factors combined exhibited departure from additivity.
Results
A significant interaction between tobacco exposure and HLA shared epitope alleles was found for the presence of ACPA as reported previously. When these interaction effects were studied for several ACPA “fine specificities,” significant interactions were noted for several citrullinated peptides. However, these interactions were not present after stratification for ACPA status, indicating that the interaction between tobacco exposure and HLA shared epitope alleles influences autoimmunity not to specific citrullinated antigens, but rather to ACPA development.
Conclusion
Our data indicate that the gene–environment interaction between HLA shared epitope alleles and smoking does not appear to shape the reactivity of the ACPA response. These data suggest that smoking promotes nonspecific citrullination rather than citrullination of specific antigens.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>21506097</pmid><doi>10.1002/art.30409</doi><tpages>10</tpages></addata></record> |
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| subjects | Adult Aged Alleles Antibodies Antigens Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Autoantibodies - genetics Autoantibodies - immunology Autoimmunity - genetics Autoimmunity - immunology Biological and medical sciences Diseases of the osteoarticular system Enzyme-Linked Immunosorbent Assay Epitopes - genetics Epitopes - immunology Female Genetic Predisposition to Disease HLA Antigens - genetics HLA Antigens - immunology Humans Immune system Immunoglobulin M - genetics Immunoglobulin M - immunology Logistic Models Male Medical sciences Middle Aged Odds Ratio Risk Factors Smoking Smoking - genetics Smoking - immunology Tobacco Tobacco, tobacco smoking Toxicology |
| title | The interaction between HLA shared epitope alleles and smoking and its contribution to autoimmunity against several citrullinated antigens |
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