类风湿性关节炎基因-基因交互作用研究进展
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摘要
迄今为止,大样本遗传关联研究尤其是全基因组关联研究(genome-wide association study,GWAS)发现并且确认了大量与类风湿性关节炎(rheumatoid arthritis,RA)遗传易感性相关的基因/区域,但是这些已经发现的遗传因素尚不足以完全解释RA的遗传度,而基因-基因交互作用是尚未被发现的遗传度的重要组成部分。实际上,基因间交互作用研究一直是RA遗传流行病学研究的一个重要方向,这类研究为深入认识RA的遗传基础和发病生物学机制提供了重要线索,也为RA发病风险预测和疾病预防提供了科学参考依据。本文将对RA基因-基因交互作用研究进展进行综述,从而为今后开展相关研究提供参考。
To date,multiple genetic susceptible genes/loci associated with rheumatoid arthritis( RA) have been identified and confirmed through large-scale genetic association studies and genome-wide association study( GWAS). However,the heritability of RA could be not fully explained by these genetic factors,and gene-gene interaction might account for part of the missing heritability. Indeed,genetic interaction study is a critical research direction in the field of genetic epidemiology of RA,and these studies have provided novel insights into the genetic basis and pathogenesis of RA. Additionally,these studies have also provided scientific reference for risk prediction and prevention of RA. This review is aimed to present a summary of recent progress in genetic interaction study of RA,thus implicate further research in this field.
To date,multiple genetic susceptible genes/loci associated with rheumatoid arthritis( RA) have been identified and confirmed through large-scale genetic association studies and genome-wide association study( GWAS). However,the heritability of RA could be not fully explained by these genetic factors,and gene-gene interaction might account for part of the missing heritability. Indeed,genetic interaction study is a critical research direction in the field of genetic epidemiology of RA,and these studies have provided novel insights into the genetic basis and pathogenesis of RA. Additionally,these studies have also provided scientific reference for risk prediction and prevention of RA. This review is aimed to present a summary of recent progress in genetic interaction study of RA,thus implicate further research in this field.
引文
[1]潘海峰,冷瑞雪,吴国翠,等.重大自身免疫性疾病的流行病学研究进展[J].中华疾病控制杂志,2018,22(11):1093-1095.DOI:10.16462/j.cnki.zhjbkz.2018.11.001.Pan HF,Leng RX,Wu GC,et al.Advance in epidemiologic studies on major autoimmune diseases[J].Chin J Dis Control Prev,2018,22(11):1093-1095.DOI:10.16462/j.cnki.zhjbkz.2018.11.001.
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[3]Sadee W,Hartmann K,Seweryn M,et al.Missing heritability of common diseases and treatments outside the protein-coding exome[J].Hum Genet,2014,133(10):1199-1215.DOI:10.1007/s00439-014-1476-7.
[4]Gregersen PK,Silver J,Winchester RJ.The shared epitope hypothesis:an approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis[J].Arthritis Rheum,1987,30(11):1205-1213.DOI:10.1002/art.178 0301102.
[5]Stanford SM,Bottini N.PTPN22:the archetypal non-HLA autoimmunity gene[J].Nat Rev Rheumatol,2014,10(10):602-611.DOI:10.1038/nrrheum.2014.109.
[6]Lee AT,Li W,Liew A,et al.The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status[J].Genes Immun,2005,6(2):129-133.DOI:10.1038/sj.gene.6364159.
[7]Costenbader KH,Chang SC,De Vivo I,et al.Genetic polymorphisms in PTPN22,PADI-4,and CTLA-4 and risk for rheumatoid arthritis in two longitudinal cohort studies:evidence of gene-environment interactions with heavy cigarette smoking[J].Arthritis Res Ther,2008,10(3):52.DOI:10.1186/ar2421.
[8]Morgan AW,Thomson W,Martin SG,et al.Reevaluation of the interaction between HLA-DRB1 shared epitope alleles,PTPN22,and smoking in determining susceptibility to autoantibody-positive and autoantibody-negative rheumatoid arthritis in a large UK Caucasian population[J].Arthritis Rheum,2009,60(9):2565-2576.DOI:10.1002/art.24752.
[9]Kallberg H,Padyukov L,Plenge RM,et al.Gene-gene and geneenvironment interactions involving HLA-DRB1,PTPN22 and smoking in two subsets of rheumatoid arthritis[J].Am J Hum Genet,2007,80(5):867-875.DOI:10.1086/516736.
[10]Mahdi H,Fisher BA,Kllberg H,et al.Specific interaction between genotype,smoking and autoimmunity to citrullinated alphaenolase in the etiology of rheumatoid arthritis[J].Nat Genet,2009,41(12):1319-1324.DOI:10.1038/ng.480.
[11]Montes A,Dieguez-Gonzalez R,Perez-Pampin E,et al.Particular association of clinical and genetic features with autoimmunity to citrullinatedα-enolase in rheumatoid arthritis[J].Arthritis Rheum,2011,63(3):654-661.DOI:10.1002/art.30357.
[12]Montes A,Perez-Pampin E,Calaza M,et al.association of anticitrullinated vimentin and anti-citrullinatedα-enolase antibodies with subsets of rheumatoid arthritis[J].Arthritis Rheum,2012,64(10):3102-3110.DOI:10.1002/art.34569.
[13]Snir O,Gomez-Cabrero D,Montes A,et al.Non-HLA genes PT-PN22,CDK6 and PADI4 are associated with specific autoantibodies in HLA-defined subgroups of rheumatoid arthritis[J].Arthritis Res Ther,2014,16(4):414.DOI:10.1186/s13075-014-0414-3.
[14]常建芳,常晓天,上官玉梦,等.PADI4在类风湿性关节炎发病中的作用[J].中华风湿病学杂志,2007,11(7):432-435.DOI:10.3760/j:issn:1007-7480.2007.07.015.Chang JF,Chang XT,ShangGuan YM,et al.The role of PADl4in the pathogenesis of rheumatoid arthritis[J].Chin J Rheumatol,2007,11(7):432-435.DOI:10.3760/j:issn:1007-7480.2007.07.015.
[15]Kang CP,Lee HS,Ju H,et al.A functional haplotype of the PA-DI4 gene associated with increased rheumatoid arthritis susceptibility in Koreans[J].Arthritis Rheum,2006,54(1):90-96.DOI:10.1002/art.21536.
[16]Bang SY,Han TU,Choi CB,et al.Peptidyl arginine deiminase type IV(PADI4)haplotypes interact with shared epitope regardless of anti-cyclic citrullinated peptide antibody or erosive joint status in rheumatoid arthritis:a case control study[J].Arthritis Res Ther,2010,12(3):115.DOI:10.1186/ar3051.
[17]Fan LY,Wang WJ,Wang Q,et al.A functional haplotype and expression of the PADI4 gene associated with increased rheumatoid arthritis susceptibility in Chinese[J].Tissue Antigens,2008,72(5):469-473.DOI:10.1111/j.1399-0039.2008.01119.x.
[18]Burr ML,Naseem H,Hinks A,et al.PADI4 genotype is not associated with rheumatoid arthritis in a large UK Caucasian population[J].Ann Rheum Dis,2010,69(4):666-670.DOI:10.1136/ard.2009.111294.
[19]Sachse C,Brockméller J,Bauer S,et al.Functional significance of a C-->A polymorphism in intron 1 of the cytochrome P450 CYP1A2gene tested with caffeine[J].Br J Clin Pharmacol,1999,47(4):445-449.DOI:10.1046/j.1365-2125.1999.00898.x.
[20]Cornelis MC,Bae SC,Kim I,et al.CYP1A2 genotype and rheumatoid arthritis in Koreans[J].Rheumatol Int,2010,30(10):1349-1354.DOI:10.1007/s00296-009-1050-0.
[21]Yun BR,El-Sohemy A,Cornelis MC,et al.Glutathione S-transferase M1,T1 and P1 genotypes and rheumatoid arthritis[J].JRheumatol,2005,32(6):992-997.DOI:10.1097/01.rhu.0000166626.68898.17.
[22]Mikuls TR,Gould KA,BynotéKK,et al.Anticitrullinated protein antibody(ACPA)in rheumatoid arthritis:influence of an interaction between HLA-DRB1 shared epitope and a deletion polymorphism in glutathione S-transferase in a cross-sectional study[J].Arthritis Res Ther,2010,12(6):213.DOI:10.1186/ar3190.
[23]Yu X,Lazarus AH.Targeting FcγRs to treat antibody-dependent autoimmunity[J].Autoimmun Rev,2016,15(6):510-512.DOI:10.1016/j.autrev.2016.02.006.
[24]Kyogoku C,Tsuchiya N,Matsuta K,et al.Studies on the association of Fc gamma receptor IIA,IIB,IIIA and IIIB polymorphisms with rheumatoid arthritis in the Japanese:evidence for a genetic interaction between HLA-DRB1 and FCGR3A[J].Genes Immun,2002,3(8):488-493.DOI:10.1038/sj.gene.6363921.
[25]Robinson JI,Barrett JH,Taylor JC,et al.Dissection of the FCGR3A association with RA:increased association in men and with autoantibody positive disease[J].Ann Rheum Dis,2010,69(6):1054-1057.DOI:10.1136/ard.2009.110874.
[26]Reith W,Leibund Gut-Landmann S,Waldburger JM.Regulation of MHC class II gene expression by the class II transactivator[J].Nat Rev Immunol,2005,5(10):793-806.DOI:10.1038/nri1708.
[27]Swanberg M,Lidman O,Padyukov L,et al.MHC2TA is associated with differential MHC molecule expression and susceptibility to rheumatoid arthritis,multiple sclerosis and myocardial infarction[J].Nat Genet,2005,37(5):486-494.DOI:10.1038/ng1544.
[28]Ronninger M,Seddighzadeh M,Eike MC,et al.Interaction analysis between HLA-DRB1 shared epitope alleles and MHC classⅡtransactivator CⅡTA gene with regard to risk of rheumatoid arthritis[J].PLo S One,2012,7(3):e32861.DOI:10.1371/journal.pone.0032861.
[29]Kochi Y,Myouzen K,Yamada R,et al.FCRL3,an autoimmune susceptibility gene,has inhibitory potential on B-cell receptor-mediated signaling[J].J Immunol,2009,183(9):5502-5510.DOI:10.4049/jimmunol.0901982.
[30]Kochi Y,Yamada R,Suzuki A,et al.A functional variant in FCRL3,encoding Fc receptor-like 3,is associated with rheumatoid arthritis and several autoimmunities[J].Nat Genet,2005,37(5):478-485.DOI:10.1038/ng1540.
[31]Newman WG,Zhang Q,Liu X,et al.Rheumatoid arthritis association with the FCRL3-169C polymorphism is restricted to PTPN221858T-homozygous individuals in a Canadian population[J].Arthritis Rheum,2006,54(12):3820-3827.DOI:10.1002/art.22270.
[32]Eyre S,Bowes J,Potter C,et al.Association of the FCRL3 gene with rheumatoid arthritis:a further example of population specificity[J].Arthritis Res Ther,2006,8(4):R117.DOI:10.1186/ar2006.
[33]Thabet MM,Wesoly J,Slagboom PE,et al.FCRL3 promoter 169CC homozygosity is associated with susceptibility to rheumatoid arthritis in Dutch Caucasians[J].Ann Rheum Dis,2007,66(6):803-806.DOI:10.1136/ard.2006.064949.
[34]Begovich AB,Chang M,Schrodi SJ.Meta-analysis evidence of a differential risk of the FCRL3-169T-->C polymorphism in white and East Asian rheumatoid arthritis patients[J].Arthritis Rheum,2007,56(9):3168-3171.DOI:10.1002/art.22857.
[35]Martínez A,Sánchez E,Valdivia A,et al.Epistatic interaction between FCRL3 and NFkappaB1 genes in Spanish patients with rheumatoid arthritis[J].Ann Rheum Dis,2006,65(9):1188-1191.DOI:10.1136/ard.2005.048454.
[36]JuliàA,Moore J,Miquel L,et al.Identification of a two-loci:epistatic interaction associated with susceptibility to rheumatoid arthritis through reverse engineering and multifactor dimensionality reduction[J].Genomics,2007,90(1):6-13.DOI:10.1016/j.ygeno.2007.03.011.
[37]Mc Kinney C,Merriman ME,Chapman PT,et al.Evidence for an influence of chemokine ligand 3-like 1(CCL3L1)gene copy number on susceptibility to rheumatoid arthritis[J].Ann Rheum Dis,2008,67(3):409-413.DOI:10.1136/ard.2007.075028.
[38]Marinou I,Walters K,Dickson MC,et al.Evidence of epistasis between interleukin 1 and selenoprotein-S with susceptibility to rheumatoid arthritis[J].Ann Rheum Dis,2009,68(9):1494-1497.DOI:10.1136/ard.2008.090001.
[39]Assmann G,Voswinkel J,Mueller M,et al.Association of rheumatoid arthritis with Mdm2 SNP309 and genetic evidence for an allele-specific interaction between MDM2 and p53 P72R variants:a case control study[J].Clin Exp Rheumatol,2009,27(4):615-619.DOI:10.1186/1471-2474-10-78.
[40]Marinou I,Till SH,Moore DJ,et al.Lack of association or interactions between the IL-4,IL-4Ralpha,IL-13 genes and rheumatoid arthritis[J].Arthritis Res Ther,2008,10(4):R80.DOI:10.1186/ar2454.
[41]Kawasaki A,Ito S,Furukawa H,et al.association of TNFAIP3interacting protein 1,TNIP1 with systemic lupus erythematosus in a Japanese population:a case-control association study[J].Arthritis Res Ther,2010,12(5):R174.DOI:10.1186/ar3134.
[42]Perdigones N,Vigo AG,Lamas JR,et al.Evidence of epistasis between TNFRSF14 and TNFRSF6B polymorphisms in patients with rheumatoid arthritis[J].Arthritis Rheum,2010,62(3):705-710.DOI:10.1002/art.27292.
[43]Deshmukh HA,Maiti AK,Kim-Howard XR,et al.Evaluation of19 autoimmune disease associated with rheumatoid arthritis in a Colombian population:evidence for replication and gene-gene interaction[J].J Rheumatol,2011,38(9):1866-1870.DOI:10.3899/jrheum.110199.
[44]Génin E,Coustet B,Allanore Y,et al.Epistatic interaction between BANK1 and BLK in rheumatoid arthritis:results from a large trans-ethnic meta-analysis[J].PLo S One,2013,8(4):e61044.DOI:10.1371/journal.pone.0061044.
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[2]Okada Y,Wu D,Trynka G,et al.Genetics of rheumatoid arthritis contributes to biology and drug discovery[J].Nature,2014,506(7488):376-381.DOI:10.1038/nature12873.
[3]Sadee W,Hartmann K,Seweryn M,et al.Missing heritability of common diseases and treatments outside the protein-coding exome[J].Hum Genet,2014,133(10):1199-1215.DOI:10.1007/s00439-014-1476-7.
[4]Gregersen PK,Silver J,Winchester RJ.The shared epitope hypothesis:an approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis[J].Arthritis Rheum,1987,30(11):1205-1213.DOI:10.1002/art.178 0301102.
[5]Stanford SM,Bottini N.PTPN22:the archetypal non-HLA autoimmunity gene[J].Nat Rev Rheumatol,2014,10(10):602-611.DOI:10.1038/nrrheum.2014.109.
[6]Lee AT,Li W,Liew A,et al.The PTPN22 R620W polymorphism associates with RF positive rheumatoid arthritis in a dose-dependent manner but not with HLA-SE status[J].Genes Immun,2005,6(2):129-133.DOI:10.1038/sj.gene.6364159.
[7]Costenbader KH,Chang SC,De Vivo I,et al.Genetic polymorphisms in PTPN22,PADI-4,and CTLA-4 and risk for rheumatoid arthritis in two longitudinal cohort studies:evidence of gene-environment interactions with heavy cigarette smoking[J].Arthritis Res Ther,2008,10(3):52.DOI:10.1186/ar2421.
[8]Morgan AW,Thomson W,Martin SG,et al.Reevaluation of the interaction between HLA-DRB1 shared epitope alleles,PTPN22,and smoking in determining susceptibility to autoantibody-positive and autoantibody-negative rheumatoid arthritis in a large UK Caucasian population[J].Arthritis Rheum,2009,60(9):2565-2576.DOI:10.1002/art.24752.
[9]Kallberg H,Padyukov L,Plenge RM,et al.Gene-gene and geneenvironment interactions involving HLA-DRB1,PTPN22 and smoking in two subsets of rheumatoid arthritis[J].Am J Hum Genet,2007,80(5):867-875.DOI:10.1086/516736.
[10]Mahdi H,Fisher BA,Kllberg H,et al.Specific interaction between genotype,smoking and autoimmunity to citrullinated alphaenolase in the etiology of rheumatoid arthritis[J].Nat Genet,2009,41(12):1319-1324.DOI:10.1038/ng.480.
[11]Montes A,Dieguez-Gonzalez R,Perez-Pampin E,et al.Particular association of clinical and genetic features with autoimmunity to citrullinatedα-enolase in rheumatoid arthritis[J].Arthritis Rheum,2011,63(3):654-661.DOI:10.1002/art.30357.
[12]Montes A,Perez-Pampin E,Calaza M,et al.association of anticitrullinated vimentin and anti-citrullinatedα-enolase antibodies with subsets of rheumatoid arthritis[J].Arthritis Rheum,2012,64(10):3102-3110.DOI:10.1002/art.34569.
[13]Snir O,Gomez-Cabrero D,Montes A,et al.Non-HLA genes PT-PN22,CDK6 and PADI4 are associated with specific autoantibodies in HLA-defined subgroups of rheumatoid arthritis[J].Arthritis Res Ther,2014,16(4):414.DOI:10.1186/s13075-014-0414-3.
[14]常建芳,常晓天,上官玉梦,等.PADI4在类风湿性关节炎发病中的作用[J].中华风湿病学杂志,2007,11(7):432-435.DOI:10.3760/j:issn:1007-7480.2007.07.015.Chang JF,Chang XT,ShangGuan YM,et al.The role of PADl4in the pathogenesis of rheumatoid arthritis[J].Chin J Rheumatol,2007,11(7):432-435.DOI:10.3760/j:issn:1007-7480.2007.07.015.
[15]Kang CP,Lee HS,Ju H,et al.A functional haplotype of the PA-DI4 gene associated with increased rheumatoid arthritis susceptibility in Koreans[J].Arthritis Rheum,2006,54(1):90-96.DOI:10.1002/art.21536.
[16]Bang SY,Han TU,Choi CB,et al.Peptidyl arginine deiminase type IV(PADI4)haplotypes interact with shared epitope regardless of anti-cyclic citrullinated peptide antibody or erosive joint status in rheumatoid arthritis:a case control study[J].Arthritis Res Ther,2010,12(3):115.DOI:10.1186/ar3051.
[17]Fan LY,Wang WJ,Wang Q,et al.A functional haplotype and expression of the PADI4 gene associated with increased rheumatoid arthritis susceptibility in Chinese[J].Tissue Antigens,2008,72(5):469-473.DOI:10.1111/j.1399-0039.2008.01119.x.
[18]Burr ML,Naseem H,Hinks A,et al.PADI4 genotype is not associated with rheumatoid arthritis in a large UK Caucasian population[J].Ann Rheum Dis,2010,69(4):666-670.DOI:10.1136/ard.2009.111294.
[19]Sachse C,Brockméller J,Bauer S,et al.Functional significance of a C-->A polymorphism in intron 1 of the cytochrome P450 CYP1A2gene tested with caffeine[J].Br J Clin Pharmacol,1999,47(4):445-449.DOI:10.1046/j.1365-2125.1999.00898.x.
[20]Cornelis MC,Bae SC,Kim I,et al.CYP1A2 genotype and rheumatoid arthritis in Koreans[J].Rheumatol Int,2010,30(10):1349-1354.DOI:10.1007/s00296-009-1050-0.
[21]Yun BR,El-Sohemy A,Cornelis MC,et al.Glutathione S-transferase M1,T1 and P1 genotypes and rheumatoid arthritis[J].JRheumatol,2005,32(6):992-997.DOI:10.1097/01.rhu.0000166626.68898.17.
[22]Mikuls TR,Gould KA,BynotéKK,et al.Anticitrullinated protein antibody(ACPA)in rheumatoid arthritis:influence of an interaction between HLA-DRB1 shared epitope and a deletion polymorphism in glutathione S-transferase in a cross-sectional study[J].Arthritis Res Ther,2010,12(6):213.DOI:10.1186/ar3190.
[23]Yu X,Lazarus AH.Targeting FcγRs to treat antibody-dependent autoimmunity[J].Autoimmun Rev,2016,15(6):510-512.DOI:10.1016/j.autrev.2016.02.006.
[24]Kyogoku C,Tsuchiya N,Matsuta K,et al.Studies on the association of Fc gamma receptor IIA,IIB,IIIA and IIIB polymorphisms with rheumatoid arthritis in the Japanese:evidence for a genetic interaction between HLA-DRB1 and FCGR3A[J].Genes Immun,2002,3(8):488-493.DOI:10.1038/sj.gene.6363921.
[25]Robinson JI,Barrett JH,Taylor JC,et al.Dissection of the FCGR3A association with RA:increased association in men and with autoantibody positive disease[J].Ann Rheum Dis,2010,69(6):1054-1057.DOI:10.1136/ard.2009.110874.
[26]Reith W,Leibund Gut-Landmann S,Waldburger JM.Regulation of MHC class II gene expression by the class II transactivator[J].Nat Rev Immunol,2005,5(10):793-806.DOI:10.1038/nri1708.
[27]Swanberg M,Lidman O,Padyukov L,et al.MHC2TA is associated with differential MHC molecule expression and susceptibility to rheumatoid arthritis,multiple sclerosis and myocardial infarction[J].Nat Genet,2005,37(5):486-494.DOI:10.1038/ng1544.
[28]Ronninger M,Seddighzadeh M,Eike MC,et al.Interaction analysis between HLA-DRB1 shared epitope alleles and MHC classⅡtransactivator CⅡTA gene with regard to risk of rheumatoid arthritis[J].PLo S One,2012,7(3):e32861.DOI:10.1371/journal.pone.0032861.
[29]Kochi Y,Myouzen K,Yamada R,et al.FCRL3,an autoimmune susceptibility gene,has inhibitory potential on B-cell receptor-mediated signaling[J].J Immunol,2009,183(9):5502-5510.DOI:10.4049/jimmunol.0901982.
[30]Kochi Y,Yamada R,Suzuki A,et al.A functional variant in FCRL3,encoding Fc receptor-like 3,is associated with rheumatoid arthritis and several autoimmunities[J].Nat Genet,2005,37(5):478-485.DOI:10.1038/ng1540.
[31]Newman WG,Zhang Q,Liu X,et al.Rheumatoid arthritis association with the FCRL3-169C polymorphism is restricted to PTPN221858T-homozygous individuals in a Canadian population[J].Arthritis Rheum,2006,54(12):3820-3827.DOI:10.1002/art.22270.
[32]Eyre S,Bowes J,Potter C,et al.Association of the FCRL3 gene with rheumatoid arthritis:a further example of population specificity[J].Arthritis Res Ther,2006,8(4):R117.DOI:10.1186/ar2006.
[33]Thabet MM,Wesoly J,Slagboom PE,et al.FCRL3 promoter 169CC homozygosity is associated with susceptibility to rheumatoid arthritis in Dutch Caucasians[J].Ann Rheum Dis,2007,66(6):803-806.DOI:10.1136/ard.2006.064949.
[34]Begovich AB,Chang M,Schrodi SJ.Meta-analysis evidence of a differential risk of the FCRL3-169T-->C polymorphism in white and East Asian rheumatoid arthritis patients[J].Arthritis Rheum,2007,56(9):3168-3171.DOI:10.1002/art.22857.
[35]Martínez A,Sánchez E,Valdivia A,et al.Epistatic interaction between FCRL3 and NFkappaB1 genes in Spanish patients with rheumatoid arthritis[J].Ann Rheum Dis,2006,65(9):1188-1191.DOI:10.1136/ard.2005.048454.
[36]JuliàA,Moore J,Miquel L,et al.Identification of a two-loci:epistatic interaction associated with susceptibility to rheumatoid arthritis through reverse engineering and multifactor dimensionality reduction[J].Genomics,2007,90(1):6-13.DOI:10.1016/j.ygeno.2007.03.011.
[37]Mc Kinney C,Merriman ME,Chapman PT,et al.Evidence for an influence of chemokine ligand 3-like 1(CCL3L1)gene copy number on susceptibility to rheumatoid arthritis[J].Ann Rheum Dis,2008,67(3):409-413.DOI:10.1136/ard.2007.075028.
[38]Marinou I,Walters K,Dickson MC,et al.Evidence of epistasis between interleukin 1 and selenoprotein-S with susceptibility to rheumatoid arthritis[J].Ann Rheum Dis,2009,68(9):1494-1497.DOI:10.1136/ard.2008.090001.
[39]Assmann G,Voswinkel J,Mueller M,et al.Association of rheumatoid arthritis with Mdm2 SNP309 and genetic evidence for an allele-specific interaction between MDM2 and p53 P72R variants:a case control study[J].Clin Exp Rheumatol,2009,27(4):615-619.DOI:10.1186/1471-2474-10-78.
[40]Marinou I,Till SH,Moore DJ,et al.Lack of association or interactions between the IL-4,IL-4Ralpha,IL-13 genes and rheumatoid arthritis[J].Arthritis Res Ther,2008,10(4):R80.DOI:10.1186/ar2454.
[41]Kawasaki A,Ito S,Furukawa H,et al.association of TNFAIP3interacting protein 1,TNIP1 with systemic lupus erythematosus in a Japanese population:a case-control association study[J].Arthritis Res Ther,2010,12(5):R174.DOI:10.1186/ar3134.
[42]Perdigones N,Vigo AG,Lamas JR,et al.Evidence of epistasis between TNFRSF14 and TNFRSF6B polymorphisms in patients with rheumatoid arthritis[J].Arthritis Rheum,2010,62(3):705-710.DOI:10.1002/art.27292.
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