Association of TNF-α gene polymorphisms with systemic lupus erythematosus in Taiwanese patients

被引：35

作者：

Lin, Y-J ^{[1
,2
,3
]}

Chen, R-H ^{[4
,5
]}

Wan, L. ^{[1
,2
,3
]}

Sheu, J. J-C ^{[1
,2
]}

Huang, C-M ^{[6
]}

Lin, C-W ^{[7
]}

Chen, S-Y ^{[1
,2
]}

Lai, C-H ^{[8
]}

Lan, Y-C ^{[9
]}

Hsueh, K-C ^{[10
]}

Tsai, C-H ^{[3
]}

Lin, T-H ^{[1
]}

Huang, Y-M ^{[1
]}

Chao, K. ^{[1
]}

Chen, D-Y ^{[1
]}

Tsai, F-J ^{[1
,2
,3
]}

机构：

[1] China Med Univ Hosp, Dept Med Res, Taichung, Taiwan

[2] China Med Univ, Grad Inst Chinese Med Sci, Taichung, Taiwan

[3] Asia Univ, Dept Biotechnol & Bioinformat, Taichung, Taiwan

[4] China Med Univ, China Med Univ Hosp, Dept Internal Med, Taichung, Taiwan

[5] China Med Univ, Coll Chinese Med, Sch Postbaccalaureate Chinese Med, Taichung, Taiwan

[6] China Med Univ Hosp, Div Rheumatol & Immunol, Taichung, Taiwan

[7] China Med Univ, Dept Med Lab Sci & Biotechnol, Taichung, Taiwan

[8] China Med Univ, Sch Med, Dept Microbiol, Taichung, Taiwan

[9] China Med Univ, Dept Hlth Risk Management, Taichung, Taiwan

[10] China Med Univ Hosp, Dept Pediat, Taichung, Taiwan

来源：

LUPUS | 2009年 / 18卷 / 11期

关键词：

single nucleotide polymorphism; systemic lupus erythematosus; tumour necrosis factor-alpha; TUMOR-NECROSIS-FACTOR; RHEUMATOID-ARTHRITIS; HAPLOTYPE RECONSTRUCTION; PROMOTER POLYMORPHISMS; MULTIPLE-SCLEROSIS; DISEASE-ACTIVITY; SUSCEPTIBILITY; SLE; POPULATION; REGION;

D O I：

10.1177/0961203309105361

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Tumour necrosis factor-alpha (TNF-alpha), an important proinflammatory cytokine, exerts a variety of physiological and pathogenic effects that lead to tissue destruction. Studies on the association of TNF-alpha genetic polymorphisms with systemic lupus erythematosus (SLE) have yielded inconclusive results. We investigated the association of TNF-alpha genetic polymorphisms (-1031T/C, -863C/A, -857T/C, -308A/G and +489A/G) with SLE in Taiwanese patients and controls. Our results indicate that 1) the frequency of the A-allele at -863 position was significantly higher in SLE patients (odds ratio = 1.46; 95% CI = 1.02-2.08); 2) the frequency of the A-allele at +489 position was significantly higher in SLE patients (odds ratio = 1.79; 95% CI = 1.21-2.65); 3) the AA or GA genotype frequencies at +489 position were significantly increased in SLE patients (AA genotype: odds ratio = 11.20; 95% CI = 1.36-92.55; GA genotype: odds ratio = 1.63; 95% CI = 1.03-2.58); 4) no significant association of TNF-alpha haplotypic distributions was observed, except for the haplotypes TCCGA, CACGA and CCCGG; and 5) the genotype frequency of the polymorphisms at -1031 was significantly different in patients with antinuclear antibodies (P = 0.022). The allele and genotype frequencies of the polymorphisms at -863 were not significantly different. The genotype frequency of the polymorphisms at -857 was significantly different in patients with haematological disorder (P = 0.025). The frequency of A allele of the polymorphisms at -308 was significantly increased in patients with malar rash (P = 0.033), discoid rash (P = 0.023), photosensitivity (P = 0.037), oral ulcers (P = 0.002) and serositis (P = 0.029). The genotype frequency of the polymorphisms at +489 was significantly different in patients with discoid rash and photosensitivity (data not shown; discoid rash, P = 0.031; photosensitivity, P = 0.044). These results suggest that TNF-alpha genetic polymorphisms contribute to SLE susceptibility in the Taiwanese population. Lupus (2009) 18, 974-979.

引用

页码：974 / 979

页数：6

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