Association of interleukin-10 promoter polymorphisms with systemic lupus erythematosus

被引:0
作者
W P Chong
W K Ip
W H-S Wong
C S Lau
T M Chan
Y L Lau
机构
[1] Queen Mary Hospital,Department of Paediatrics and Adolescent Medicine
[2] The University of Hong Kong,Department of Medicine
[3] Queen Mary Hospital,undefined
[4] The University of Hong Kong,undefined
来源
Genes & Immunity | 2004年 / 5卷
关键词
systemic lupus erythematosus; interleukin 10; polymorphism; haplotype;
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摘要
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 ⩽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.
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页码:484 / 492
页数:8
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共 204 条
[1]  
Shlomchik MJ(2001)From T to B and back again: positive feedback in systemic autoimmune disease Nat Rev Immunol 1 147-153
[2]  
Craft JE(1992)A revised estimate of twin concordance in systemic lupus erythematosus Arthritis Rheum 35 311-318
[3]  
Mamula MJ(1987)A family survey of lupus erythematosus. 1. Heritability J Rheumatol 14 867-869
[4]  
Deapen D(1996)Genetic basis of systemic lupus erythematosus Curr Opin Immunol 8 843-851
[5]  
Escalante A(1994)Polygenic control of susceptibility to murine systemic lupus erythematosus Immunity 1 219-229
[6]  
Weinrib L(1999)Genetic dissection of systemic lupus erythematosus Curr Opin Immunol 11 701-707
[7]  
Lawrence JS(2002)The genetics of systemic lupus erythematosus: putting the pieces together Genes Immun 3 S71-S85
[8]  
Martins CL(1987)Strong association between the major histocompatibility complex and systemic lupus erythematosus in Southern Chinese J Rheumatol 14 1128-1131
[9]  
Drake GL(1996)Mannose-binding protein in Chinese patients with systemic lupus erythematosus Arthritis Rheum 39 706-708
[10]  
Vyse TJ(1998)Association of systemic lupus erythematosus with promoter polymorphisms of the mannose-binding lectin gene Arthritis Rheum 41 1663-1668