Polymorphisms of the CTLA-4 exon 1 and promoter gene in systemic lupus erythematosus

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Abstract

The objective of this study was to determine whether the polymorphisms of the CTLA-4 exon 1 (+49) and promoter (-318) are associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) in 80 SLE patients and 86 healthy control subjects. The genotype distribution of the CTLA- 4 exon 1 (+49) differed between SLE patients and controls (x2 = 6.74, 2 degrees of freedom (d.f.), P= 0.03). The CTLA-4 AG genotype occurred more frequently in patients with SLE (46.3% vs 33.7% controls). On the other hand, the CTLA-4 AA genotype as well as the CTLA-4 GG genotype was less frequent among SLE patients than among control subjects (1.3% vs 9.3% and 52.5% vs 57.0%, respectively). The genotype distribution of the CTLA-4 promoter (-318) differed between SLE patients and control subjects (CT, TT, CC; genotypes 27.5%, 0%, 72.5% vs 16.3%, 4.7%, 79.1% controls respectively, x2=6.36, 2 d.f., P = 0.04). However, Fischer's exact or x2 P-values for each genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) between SLE and control group were > 0.05. Clinically, in the lupus patients there was no significant difference according to the CTLA-4 polymorphisms. In conclusion, no correlation was found between CTLA-4 exon 1 (+49) and promoter (-318) polymorphisms and SLE in our study.

Original languageEnglish
Pages (from-to)601-605
Number of pages5
JournalLupus
Volume10
Issue number9
DOIs
Publication statusPublished - 2001 Oct 23

Fingerprint

Systemic Lupus Erythematosus
Exons
Genotype
Genes
Restriction Fragment Length Polymorphisms
Healthy Volunteers
Polymerase Chain Reaction
Control Groups
DNA

Keywords

  • CTLA-4
  • Polymorphisms
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Rheumatology

Cite this

Polymorphisms of the CTLA-4 exon 1 and promoter gene in systemic lupus erythematosus. / Lee, Young Ho; Kim, Y. R.; Ji, Jong Dae; Sohn, Jeongwon; Song, Gwan Gyu.

In: Lupus, Vol. 10, No. 9, 23.10.2001, p. 601-605.

Research output: Contribution to journalArticle

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abstract = "The objective of this study was to determine whether the polymorphisms of the CTLA-4 exon 1 (+49) and promoter (-318) are associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) in 80 SLE patients and 86 healthy control subjects. The genotype distribution of the CTLA- 4 exon 1 (+49) differed between SLE patients and controls (x2 = 6.74, 2 degrees of freedom (d.f.), P= 0.03). The CTLA-4 AG genotype occurred more frequently in patients with SLE (46.3{\%} vs 33.7{\%} controls). On the other hand, the CTLA-4 AA genotype as well as the CTLA-4 GG genotype was less frequent among SLE patients than among control subjects (1.3{\%} vs 9.3{\%} and 52.5{\%} vs 57.0{\%}, respectively). The genotype distribution of the CTLA-4 promoter (-318) differed between SLE patients and control subjects (CT, TT, CC; genotypes 27.5{\%}, 0{\%}, 72.5{\%} vs 16.3{\%}, 4.7{\%}, 79.1{\%} controls respectively, x2=6.36, 2 d.f., P = 0.04). However, Fischer's exact or x2 P-values for each genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) between SLE and control group were > 0.05. Clinically, in the lupus patients there was no significant difference according to the CTLA-4 polymorphisms. In conclusion, no correlation was found between CTLA-4 exon 1 (+49) and promoter (-318) polymorphisms and SLE in our study.",
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N2 - The objective of this study was to determine whether the polymorphisms of the CTLA-4 exon 1 (+49) and promoter (-318) are associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) in 80 SLE patients and 86 healthy control subjects. The genotype distribution of the CTLA- 4 exon 1 (+49) differed between SLE patients and controls (x2 = 6.74, 2 degrees of freedom (d.f.), P= 0.03). The CTLA-4 AG genotype occurred more frequently in patients with SLE (46.3% vs 33.7% controls). On the other hand, the CTLA-4 AA genotype as well as the CTLA-4 GG genotype was less frequent among SLE patients than among control subjects (1.3% vs 9.3% and 52.5% vs 57.0%, respectively). The genotype distribution of the CTLA-4 promoter (-318) differed between SLE patients and control subjects (CT, TT, CC; genotypes 27.5%, 0%, 72.5% vs 16.3%, 4.7%, 79.1% controls respectively, x2=6.36, 2 d.f., P = 0.04). However, Fischer's exact or x2 P-values for each genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) between SLE and control group were > 0.05. Clinically, in the lupus patients there was no significant difference according to the CTLA-4 polymorphisms. In conclusion, no correlation was found between CTLA-4 exon 1 (+49) and promoter (-318) polymorphisms and SLE in our study.

AB - The objective of this study was to determine whether the polymorphisms of the CTLA-4 exon 1 (+49) and promoter (-318) are associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) in 80 SLE patients and 86 healthy control subjects. The genotype distribution of the CTLA- 4 exon 1 (+49) differed between SLE patients and controls (x2 = 6.74, 2 degrees of freedom (d.f.), P= 0.03). The CTLA-4 AG genotype occurred more frequently in patients with SLE (46.3% vs 33.7% controls). On the other hand, the CTLA-4 AA genotype as well as the CTLA-4 GG genotype was less frequent among SLE patients than among control subjects (1.3% vs 9.3% and 52.5% vs 57.0%, respectively). The genotype distribution of the CTLA-4 promoter (-318) differed between SLE patients and control subjects (CT, TT, CC; genotypes 27.5%, 0%, 72.5% vs 16.3%, 4.7%, 79.1% controls respectively, x2=6.36, 2 d.f., P = 0.04). However, Fischer's exact or x2 P-values for each genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) between SLE and control group were > 0.05. Clinically, in the lupus patients there was no significant difference according to the CTLA-4 polymorphisms. In conclusion, no correlation was found between CTLA-4 exon 1 (+49) and promoter (-318) polymorphisms and SLE in our study.

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