Disease association of two distinct interleukin-18 promoter polymorphisms in Caucasian rheumatoid arthritis patients
Interleukin (IL)-18 is an important mediator of innate and adaptive immunity. We searched for an association of IL-18 promoter single-nucleotide polymorphisms (SNP) with rheumatoid arthritis (RA) in Caucasians. The entire study population was composed of two independent cohorts from Germany ( n =200...
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| Veröffentlicht in: | Genes and immunity 2005-05, Vol.6 (3), p.211-216 |
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| creator | Gracie, J A Koyama, N Murdoch, J Field, M McGarry, F Crilly, A Schobel, A Madhok, R Pons-Kühnemann, J McInnes, I B Möller, B |
| description | Interleukin (IL)-18 is an important mediator of innate and adaptive immunity. We searched for an association of IL-18 promoter single-nucleotide polymorphisms (SNP) with rheumatoid arthritis (RA) in Caucasians. The entire study population was composed of two independent cohorts from Germany (
n
=200) and Scotland (
n
=410). Presence of IL-18 SNP at positions −607 and −137 was determined by allele-specific PCR in 327 RA patients and 283 healthy donors (HD). Diplotype distributions of both loci were in Hardy–Weinberg equilibrium (HWE) in the German and Scottish HD cohorts. In contrast, locus −607 was in HW disequilibrium in German, and locus −137 in Scottish RA patients. Diplotypic exact χ
2
tests suggested that −607CC was overrepresented in German, and −137CC in Scottish RA patients, but conservative χ
2
trend analyses could not prove any significant disease association of these single loci. SNP −607 and −137 were in strong linkage disequilibrium. The −607C
*
−137C haplotype was more prevalent in German RA (3.2 vs 1.2%) and in Scottish RA patients (4.1 vs 0.9%) than in the respective HD cohorts. These observations suggest that SNP of both positions contribute to the genetic background of RA pathogenesis. |
| doi_str_mv | 10.1038/sj.gene.6364183 |
| format | Article |
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n
=200) and Scotland (
n
=410). Presence of IL-18 SNP at positions −607 and −137 was determined by allele-specific PCR in 327 RA patients and 283 healthy donors (HD). Diplotype distributions of both loci were in Hardy–Weinberg equilibrium (HWE) in the German and Scottish HD cohorts. In contrast, locus −607 was in HW disequilibrium in German, and locus −137 in Scottish RA patients. Diplotypic exact χ
2
tests suggested that −607CC was overrepresented in German, and −137CC in Scottish RA patients, but conservative χ
2
trend analyses could not prove any significant disease association of these single loci. SNP −607 and −137 were in strong linkage disequilibrium. The −607C
*
−137C haplotype was more prevalent in German RA (3.2 vs 1.2%) and in Scottish RA patients (4.1 vs 0.9%) than in the respective HD cohorts. These observations suggest that SNP of both positions contribute to the genetic background of RA pathogenesis.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6364183</identifier><identifier>PMID: 15789055</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adaptive immunity ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Care and treatment ; Cytokines ; Disease ; European Continental Ancestry Group ; full-paper ; Gene Expression ; Genes ; Genetic aspects ; Genetic polymorphisms ; Germany ; Haplotypes ; Human Genetics ; Humans ; Immunology ; Interleukin 18 ; Interleukin-18 - genetics ; Interleukin-18 - metabolism ; Interleukins ; Linkage disequilibrium ; Lymphocytes ; Pathogenesis ; Physiological aspects ; Polymorphism ; Polymorphism, Genetic ; Population studies ; Promoter Regions, Genetic ; Rheumatoid arthritis ; Risk factors ; Scotland ; Single-nucleotide polymorphism ; Statistical significance ; Tumor necrosis factor-TNF ; White people</subject><ispartof>Genes and immunity, 2005-05, Vol.6 (3), p.211-216</ispartof><rights>Springer Nature Limited 2005</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c564t-fdbe8823bfafcb7b808481ee6710bdef4df27e5e1fff90c169450e3c6681c4f23</citedby><cites>FETCH-LOGICAL-c564t-fdbe8823bfafcb7b808481ee6710bdef4df27e5e1fff90c169450e3c6681c4f23</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.6364183$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6364183$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15789055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gracie, J A</creatorcontrib><creatorcontrib>Koyama, N</creatorcontrib><creatorcontrib>Murdoch, J</creatorcontrib><creatorcontrib>Field, M</creatorcontrib><creatorcontrib>McGarry, F</creatorcontrib><creatorcontrib>Crilly, A</creatorcontrib><creatorcontrib>Schobel, A</creatorcontrib><creatorcontrib>Madhok, R</creatorcontrib><creatorcontrib>Pons-Kühnemann, J</creatorcontrib><creatorcontrib>McInnes, I B</creatorcontrib><creatorcontrib>Möller, B</creatorcontrib><title>Disease association of two distinct interleukin-18 promoter polymorphisms in Caucasian rheumatoid arthritis patients</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Interleukin (IL)-18 is an important mediator of innate and adaptive immunity. We searched for an association of IL-18 promoter single-nucleotide polymorphisms (SNP) with rheumatoid arthritis (RA) in Caucasians. The entire study population was composed of two independent cohorts from Germany (
n
=200) and Scotland (
n
=410). Presence of IL-18 SNP at positions −607 and −137 was determined by allele-specific PCR in 327 RA patients and 283 healthy donors (HD). Diplotype distributions of both loci were in Hardy–Weinberg equilibrium (HWE) in the German and Scottish HD cohorts. In contrast, locus −607 was in HW disequilibrium in German, and locus −137 in Scottish RA patients. Diplotypic exact χ
2
tests suggested that −607CC was overrepresented in German, and −137CC in Scottish RA patients, but conservative χ
2
trend analyses could not prove any significant disease association of these single loci. SNP −607 and −137 were in strong linkage disequilibrium. The −607C
*
−137C haplotype was more prevalent in German RA (3.2 vs 1.2%) and in Scottish RA patients (4.1 vs 0.9%) than in the respective HD cohorts. These observations suggest that SNP of both positions contribute to the genetic background of RA pathogenesis.</description><subject>Adaptive immunity</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Care and treatment</subject><subject>Cytokines</subject><subject>Disease</subject><subject>European Continental Ancestry Group</subject><subject>full-paper</subject><subject>Gene Expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Germany</subject><subject>Haplotypes</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Interleukin 18</subject><subject>Interleukin-18 - genetics</subject><subject>Interleukin-18 - metabolism</subject><subject>Interleukins</subject><subject>Linkage disequilibrium</subject><subject>Lymphocytes</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Population studies</subject><subject>Promoter Regions, Genetic</subject><subject>Rheumatoid arthritis</subject><subject>Risk factors</subject><subject>Scotland</subject><subject>Single-nucleotide polymorphism</subject><subject>Statistical significance</subject><subject>Tumor necrosis factor-TNF</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>BENPR</sourceid><recordid>eNqFkt2L1DAUxYso7rr67JsUFwQfOpu0aZI-LuPXwoLgx3NI05vZjG0y5qbo_vemzMAw4iJ5SLj53XNzyCmKl5SsKGnkFW5XG_Cw4g1nVDaPinPKBK9aJsjj5cx5xaTozopniFtCKKe8e1qc0VbIjrTteZHeOQSNUGrEYJxOLvgy2DL9CuXgMDlvUul8gjjC_MP5ispyF8MUcqXchfF-CnF353DCTJVrPRuNTvsy3sE86RTcUOqY7qJLDstdlgef8HnxxOoR4cVhvyi-f3j_bf2puv388WZ9fVuZlrNU2aEHKeumt9qaXvSSSCYpABeU9ANYNthaQAvUWtsRk62xlkBjOJfUMFs3F8WbvW5-8c8ZMKnJoYFx1B7CjIoLIXlDxX9BKtqG1WwBL_8Ct2GOPptQdf4BwUjT0Ey9fpCiUnYtaelRaqNHUM7bkKI2y1x1TWXd1R2Ry8DVP6i8BpicCR6sy_WThrcnDZlJ8Dtt9Iyobr5-OWWv9qyJATGCVbvoJh3vFSVqyZfCrVrypQ75yh2vDs7mfoLhyB8ClQGyBzBf-Q3Eo_WHNP8AJX_cmw</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>Gracie, J A</creator><creator>Koyama, N</creator><creator>Murdoch, J</creator><creator>Field, M</creator><creator>McGarry, F</creator><creator>Crilly, A</creator><creator>Schobel, A</creator><creator>Madhok, R</creator><creator>Pons-Kühnemann, J</creator><creator>McInnes, I B</creator><creator>Möller, B</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>20050501</creationdate><title>Disease association of two distinct interleukin-18 promoter polymorphisms in Caucasian rheumatoid arthritis patients</title><author>Gracie, J A ; Koyama, N ; Murdoch, J ; Field, M ; McGarry, F ; Crilly, A ; Schobel, A ; Madhok, R ; Pons-Kühnemann, J ; McInnes, I B ; Möller, B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-fdbe8823bfafcb7b808481ee6710bdef4df27e5e1fff90c169450e3c6681c4f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adaptive immunity</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Care and treatment</topic><topic>Cytokines</topic><topic>Disease</topic><topic>European Continental Ancestry Group</topic><topic>full-paper</topic><topic>Gene Expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Germany</topic><topic>Haplotypes</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Interleukin 18</topic><topic>Interleukin-18 - genetics</topic><topic>Interleukin-18 - metabolism</topic><topic>Interleukins</topic><topic>Linkage disequilibrium</topic><topic>Lymphocytes</topic><topic>Pathogenesis</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Population studies</topic><topic>Promoter Regions, Genetic</topic><topic>Rheumatoid arthritis</topic><topic>Risk factors</topic><topic>Scotland</topic><topic>Single-nucleotide polymorphism</topic><topic>Statistical significance</topic><topic>Tumor necrosis factor-TNF</topic><topic>White people</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gracie, J A</creatorcontrib><creatorcontrib>Koyama, N</creatorcontrib><creatorcontrib>Murdoch, J</creatorcontrib><creatorcontrib>Field, M</creatorcontrib><creatorcontrib>McGarry, F</creatorcontrib><creatorcontrib>Crilly, A</creatorcontrib><creatorcontrib>Schobel, A</creatorcontrib><creatorcontrib>Madhok, R</creatorcontrib><creatorcontrib>Pons-Kühnemann, J</creatorcontrib><creatorcontrib>McInnes, I B</creatorcontrib><creatorcontrib>Möller, B</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</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>Gracie, J A</au><au>Koyama, N</au><au>Murdoch, J</au><au>Field, M</au><au>McGarry, F</au><au>Crilly, A</au><au>Schobel, A</au><au>Madhok, R</au><au>Pons-Kühnemann, J</au><au>McInnes, I B</au><au>Möller, B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disease association of two distinct interleukin-18 promoter polymorphisms in Caucasian rheumatoid arthritis patients</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>6</volume><issue>3</issue><spage>211</spage><epage>216</epage><pages>211-216</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Interleukin (IL)-18 is an important mediator of innate and adaptive immunity. We searched for an association of IL-18 promoter single-nucleotide polymorphisms (SNP) with rheumatoid arthritis (RA) in Caucasians. The entire study population was composed of two independent cohorts from Germany (
n
=200) and Scotland (
n
=410). Presence of IL-18 SNP at positions −607 and −137 was determined by allele-specific PCR in 327 RA patients and 283 healthy donors (HD). Diplotype distributions of both loci were in Hardy–Weinberg equilibrium (HWE) in the German and Scottish HD cohorts. In contrast, locus −607 was in HW disequilibrium in German, and locus −137 in Scottish RA patients. Diplotypic exact χ
2
tests suggested that −607CC was overrepresented in German, and −137CC in Scottish RA patients, but conservative χ
2
trend analyses could not prove any significant disease association of these single loci. SNP −607 and −137 were in strong linkage disequilibrium. The −607C
*
−137C haplotype was more prevalent in German RA (3.2 vs 1.2%) and in Scottish RA patients (4.1 vs 0.9%) than in the respective HD cohorts. These observations suggest that SNP of both positions contribute to the genetic background of RA pathogenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15789055</pmid><doi>10.1038/sj.gene.6364183</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptive immunity Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - metabolism Biomedical and Life Sciences Biomedicine Cancer Research Care and treatment Cytokines Disease European Continental Ancestry Group full-paper Gene Expression Genes Genetic aspects Genetic polymorphisms Germany Haplotypes Human Genetics Humans Immunology Interleukin 18 Interleukin-18 - genetics Interleukin-18 - metabolism Interleukins Linkage disequilibrium Lymphocytes Pathogenesis Physiological aspects Polymorphism Polymorphism, Genetic Population studies Promoter Regions, Genetic Rheumatoid arthritis Risk factors Scotland Single-nucleotide polymorphism Statistical significance Tumor necrosis factor-TNF White people |
| title | Disease association of two distinct interleukin-18 promoter polymorphisms in Caucasian rheumatoid arthritis patients |
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