Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus
Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A, -2849G/A, -2763C/A, -1082A/G, -819T/C and -592A/C) and micros...
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| Veröffentlicht in: | Genes and immunity 2004-09, Vol.5 (6), p.484-492 |
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| description | Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A, -2849G/A, -2763C/A, -1082A/G, -819T/C and -592A/C) and microsatellites (IL10.R, IL10.G) with SLE in 554 Hong Kong Chinese patients and 708 ethnically matched controls. Six haplotypes (hts) were identified from the SNPs. The genotype distribution of the ht1 (T-C-A-T-A), which is associated with low IL-10 production, was different in patients and controls (P=0.009). The homozygous genotype of non-ht1 was significantly increased in patients (P=0.009, odds ratio (OR)=1.80, 95% CI: 1.15-2.82). The frequency of IL10.G4 of IL10.G was also significantly increased in patients (P=0.017, OR=2.53, 95% CI: 1.18-5.40). We found that the homozygous non-ht1 combined with short allele (CA repeat number < or =21) of IL10.G has a dose-dependent effect on SLE susceptibility: non-ht1/non-ht1 with homozygous short allele showed a higher OR (OR=4.11, 95% CI: 1.27-13.2, P=0.018) of association with SLE than the genotype of non-ht1/non-ht1 with heterozygous short/long allele (OR=2.98, 95% CI: 1.26-7.07, P=0.013) and homozygous long allele (OR=1.05, 95% CI: 0.62-1.78, P=0.848). The frequency of non-ht1 was significantly increased in patients with serositis (P |
| doi_str_mv | 10.1038/sj.gene.6364119 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_66835080</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A182930162</galeid><sourcerecordid>A182930162</sourcerecordid><originalsourceid>FETCH-LOGICAL-c597t-e648df3d56adfa71e5917a26b27c85efb2eb22e2718253f2ce611ae50abe3b4c3</originalsourceid><addsrcrecordid>eNqFktuL1DAUxoso7rr67JNSFAQfOptLc-njsHhZWBC8vYa0PZ3J2DbdnBSd_96UGV1GFMlDwuH3neQ7-bLsKSUrSri-xN1qAyOsJJclpdW97JyWShaiVOT-cpayKLWqzrJHiDtCqKSyepidUcEqIRk9z76uEX3jbHR-zH2XuzFC6GH-5saCknwKfvCpkk--3w8-TFuHA-bfXdzmuMcIg2vyfp5mzCHs4xYGGz3O-Dh70Nke4clxv8i-vH3z-ep9cfPh3fXV-qZoRKViAbLUbcdbIW3bWUVBVFRZJmumGi2gqxnUjAFTVDPBO9aApNSCILYGXpcNv8heHfqmh97OgNEMDhvoezuCn9FIqbkgmvwXpEpxJRRN4Ms_wJ2fw5hMGJZmrBgneqFe_JOiWistZHnXamN7MG7sfAy2We4162So4uk_WKJWf6HSapfh-hE6l-ongtcngsRE-BE3dkY0158-nrKXB7YJHjFAZ6bgBhv2hhKzJMjgziwJMscEJcXzo7O5HqC944-RScCzAzDaOAf4Dfxq8BMFn8qQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>218878564</pqid></control><display><type>article</type><title>Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Chong, W P ; Ip, W K ; Wong, W H-S ; Lau, C S ; Chan, T M ; Lau, Y L</creator><creatorcontrib>Chong, W P ; Ip, W K ; Wong, W H-S ; Lau, C S ; Chan, T M ; Lau, Y L</creatorcontrib><description>Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A, -2849G/A, -2763C/A, -1082A/G, -819T/C and -592A/C) and microsatellites (IL10.R, IL10.G) with SLE in 554 Hong Kong Chinese patients and 708 ethnically matched controls. Six haplotypes (hts) were identified from the SNPs. The genotype distribution of the ht1 (T-C-A-T-A), which is associated with low IL-10 production, was different in patients and controls (P=0.009). The homozygous genotype of non-ht1 was significantly increased in patients (P=0.009, odds ratio (OR)=1.80, 95% CI: 1.15-2.82). The frequency of IL10.G4 of IL10.G was also significantly increased in patients (P=0.017, OR=2.53, 95% CI: 1.18-5.40). We found that the homozygous non-ht1 combined with short allele (CA repeat number < or =21) of IL10.G has a dose-dependent effect on SLE susceptibility: non-ht1/non-ht1 with homozygous short allele showed a higher OR (OR=4.11, 95% CI: 1.27-13.2, P=0.018) of association with SLE than the genotype of non-ht1/non-ht1 with heterozygous short/long allele (OR=2.98, 95% CI: 1.26-7.07, P=0.013) and homozygous long allele (OR=1.05, 95% CI: 0.62-1.78, P=0.848). The frequency of non-ht1 was significantly increased in patients with serositis (P<0.0001, OR=2.42, 95% CI: 1.55-3.80). In conclusion, the high expression promoter genotype is associated with SLE in Chinese.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6364119</identifier><identifier>PMID: 15295621</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Adult ; Alleles ; Binding sites ; China ; Cytokines ; Female ; Gene Frequency ; Genes ; Genetic aspects ; Genetic polymorphisms ; Genotype ; Genotype & phenotype ; Haplotypes ; Haplotypes - genetics ; Health aspects ; Heterozygote ; Homozygote ; Humans ; Hyperactivity ; Interleukin 1 ; Interleukin 10 ; Interleukin-10 - genetics ; Lupus ; Lupus Erythematosus, Systemic - genetics ; Male ; Microsatellite Repeats - genetics ; Microsatellites ; Polymorphism ; Polymorphism, Single Nucleotide - genetics ; Promoter Regions, Genetic - genetics ; Serositis ; Single-nucleotide polymorphism ; Systemic lupus erythematosus ; Tumor necrosis factor-TNF</subject><ispartof>Genes and immunity, 2004-09, Vol.5 (6), p.484-492</ispartof><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c597t-e648df3d56adfa71e5917a26b27c85efb2eb22e2718253f2ce611ae50abe3b4c3</citedby><cites>FETCH-LOGICAL-c597t-e648df3d56adfa71e5917a26b27c85efb2eb22e2718253f2ce611ae50abe3b4c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27933,27934</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15295621$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chong, W P</creatorcontrib><creatorcontrib>Ip, W K</creatorcontrib><creatorcontrib>Wong, W H-S</creatorcontrib><creatorcontrib>Lau, C S</creatorcontrib><creatorcontrib>Chan, T M</creatorcontrib><creatorcontrib>Lau, Y L</creatorcontrib><title>Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><description>Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A, -2849G/A, -2763C/A, -1082A/G, -819T/C and -592A/C) and microsatellites (IL10.R, IL10.G) with SLE in 554 Hong Kong Chinese patients and 708 ethnically matched controls. Six haplotypes (hts) were identified from the SNPs. The genotype distribution of the ht1 (T-C-A-T-A), which is associated with low IL-10 production, was different in patients and controls (P=0.009). The homozygous genotype of non-ht1 was significantly increased in patients (P=0.009, odds ratio (OR)=1.80, 95% CI: 1.15-2.82). The frequency of IL10.G4 of IL10.G was also significantly increased in patients (P=0.017, OR=2.53, 95% CI: 1.18-5.40). We found that the homozygous non-ht1 combined with short allele (CA repeat number < or =21) of IL10.G has a dose-dependent effect on SLE susceptibility: non-ht1/non-ht1 with homozygous short allele showed a higher OR (OR=4.11, 95% CI: 1.27-13.2, P=0.018) of association with SLE than the genotype of non-ht1/non-ht1 with heterozygous short/long allele (OR=2.98, 95% CI: 1.26-7.07, P=0.013) and homozygous long allele (OR=1.05, 95% CI: 0.62-1.78, P=0.848). The frequency of non-ht1 was significantly increased in patients with serositis (P<0.0001, OR=2.42, 95% CI: 1.55-3.80). In conclusion, the high expression promoter genotype is associated with SLE in Chinese.</description><subject>Adult</subject><subject>Alleles</subject><subject>Binding sites</subject><subject>China</subject><subject>Cytokines</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Haplotypes</subject><subject>Haplotypes - genetics</subject><subject>Health aspects</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Hyperactivity</subject><subject>Interleukin 1</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - genetics</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - genetics</subject><subject>Male</subject><subject>Microsatellite Repeats - genetics</subject><subject>Microsatellites</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Serositis</subject><subject>Single-nucleotide polymorphism</subject><subject>Systemic lupus erythematosus</subject><subject>Tumor necrosis factor-TNF</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</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>eNqFktuL1DAUxoso7rr67JNSFAQfOptLc-njsHhZWBC8vYa0PZ3J2DbdnBSd_96UGV1GFMlDwuH3neQ7-bLsKSUrSri-xN1qAyOsJJclpdW97JyWShaiVOT-cpayKLWqzrJHiDtCqKSyepidUcEqIRk9z76uEX3jbHR-zH2XuzFC6GH-5saCknwKfvCpkk--3w8-TFuHA-bfXdzmuMcIg2vyfp5mzCHs4xYGGz3O-Dh70Nke4clxv8i-vH3z-ep9cfPh3fXV-qZoRKViAbLUbcdbIW3bWUVBVFRZJmumGi2gqxnUjAFTVDPBO9aApNSCILYGXpcNv8heHfqmh97OgNEMDhvoezuCn9FIqbkgmvwXpEpxJRRN4Ms_wJ2fw5hMGJZmrBgneqFe_JOiWistZHnXamN7MG7sfAy2We4162So4uk_WKJWf6HSapfh-hE6l-ongtcngsRE-BE3dkY0158-nrKXB7YJHjFAZ6bgBhv2hhKzJMjgziwJMscEJcXzo7O5HqC944-RScCzAzDaOAf4Dfxq8BMFn8qQ</recordid><startdate>20040901</startdate><enddate>20040901</enddate><creator>Chong, W P</creator><creator>Ip, W K</creator><creator>Wong, W H-S</creator><creator>Lau, C S</creator><creator>Chan, T M</creator><creator>Lau, Y L</creator><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>20040901</creationdate><title>Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus</title><author>Chong, W P ; Ip, W K ; Wong, W H-S ; Lau, C S ; Chan, T M ; Lau, Y L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c597t-e648df3d56adfa71e5917a26b27c85efb2eb22e2718253f2ce611ae50abe3b4c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Binding sites</topic><topic>China</topic><topic>Cytokines</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Haplotypes</topic><topic>Haplotypes - genetics</topic><topic>Health aspects</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Hyperactivity</topic><topic>Interleukin 1</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - genetics</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - genetics</topic><topic>Male</topic><topic>Microsatellite Repeats - genetics</topic><topic>Microsatellites</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Serositis</topic><topic>Single-nucleotide polymorphism</topic><topic>Systemic lupus erythematosus</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chong, W P</creatorcontrib><creatorcontrib>Ip, W K</creatorcontrib><creatorcontrib>Wong, W H-S</creatorcontrib><creatorcontrib>Lau, C S</creatorcontrib><creatorcontrib>Chan, T M</creatorcontrib><creatorcontrib>Lau, Y L</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>Chong, W P</au><au>Ip, W K</au><au>Wong, W H-S</au><au>Lau, C S</au><au>Chan, T M</au><au>Lau, Y L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus</atitle><jtitle>Genes and immunity</jtitle><addtitle>Genes Immun</addtitle><date>2004-09-01</date><risdate>2004</risdate><volume>5</volume><issue>6</issue><spage>484</spage><epage>492</epage><pages>484-492</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A, -2849G/A, -2763C/A, -1082A/G, -819T/C and -592A/C) and microsatellites (IL10.R, IL10.G) with SLE in 554 Hong Kong Chinese patients and 708 ethnically matched controls. Six haplotypes (hts) were identified from the SNPs. The genotype distribution of the ht1 (T-C-A-T-A), which is associated with low IL-10 production, was different in patients and controls (P=0.009). The homozygous genotype of non-ht1 was significantly increased in patients (P=0.009, odds ratio (OR)=1.80, 95% CI: 1.15-2.82). The frequency of IL10.G4 of IL10.G was also significantly increased in patients (P=0.017, OR=2.53, 95% CI: 1.18-5.40). We found that the homozygous non-ht1 combined with short allele (CA repeat number < or =21) of IL10.G has a dose-dependent effect on SLE susceptibility: non-ht1/non-ht1 with homozygous short allele showed a higher OR (OR=4.11, 95% CI: 1.27-13.2, P=0.018) of association with SLE than the genotype of non-ht1/non-ht1 with heterozygous short/long allele (OR=2.98, 95% CI: 1.26-7.07, P=0.013) and homozygous long allele (OR=1.05, 95% CI: 0.62-1.78, P=0.848). The frequency of non-ht1 was significantly increased in patients with serositis (P<0.0001, OR=2.42, 95% CI: 1.55-3.80). In conclusion, the high expression promoter genotype is associated with SLE in Chinese.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>15295621</pmid><doi>10.1038/sj.gene.6364119</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Alleles Binding sites China Cytokines Female Gene Frequency Genes Genetic aspects Genetic polymorphisms Genotype Genotype & phenotype Haplotypes Haplotypes - genetics Health aspects Heterozygote Homozygote Humans Hyperactivity Interleukin 1 Interleukin 10 Interleukin-10 - genetics Lupus Lupus Erythematosus, Systemic - genetics Male Microsatellite Repeats - genetics Microsatellites Polymorphism Polymorphism, Single Nucleotide - genetics Promoter Regions, Genetic - genetics Serositis Single-nucleotide polymorphism Systemic lupus erythematosus Tumor necrosis factor-TNF |
| title | Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus |
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