Single nucleotide polymorphisms of the inflammatory cytokine genes in adults with chronic immune thrombocytopenic purpura

Takashi Satoh, Janardan P. Pandey, Yuka Okazaki, Hidekata Yasuoka, Yutaka Kawakami, Yasuo Ikeda, Masataka Kuwana

研究成果: Article

38 引用 (Scopus)

抄録

Single nucleotide polymorphisms (SNPs) of inflammatory cytokine genes were examined in 84 adult Japanese patients with chronic immune thrombocytopenic purpura (ITP) and 56 race-matched healthy controls. The SNPs examined were within the genes encoding tumour necrosis factor (TNF)-α (-238 G/A and -308 G/A), TNF-β (+252 G/A), and interleukin (IL)-1β (-511 C/T and +3953 T/C). Of these SNPs, the frequency of the TNF-β (+252) G/G phenotype was significantly higher in ITP patients than in healthy controls (21% vs. 7%, P = 0.04, odds ratio = 3.6, 95% confidence interval 1.1-11.1), while no significant association was detected for the other SNPs. The distribution of the TNF-β (+252) phenotype was not associated with human leucocyte antigen class II alleles or the therapeutic response in ITP patients. The frequency of circulating anti-glycoprotein IIb/IIIa antibody-producing B cells was significantly higher in ITP patients with the TNF-β (+252) G/G phenotype than in those with the G/A or A/A phenotype (11.9 ± 4.9 vs. 6.8 ± 4.9 and 3.7 ± 2.8 per 105 peripheral blood mononuclear cells; P = 0.02 and P < 0.001, respectively). These findings suggest that the SNP located at TNF-β (+252) contributes to susceptibility to chronic ITP by controlling the autoreactive B-cell responses to platelet membrane glycoproteins.

元の言語English
ページ(範囲)796-801
ページ数6
ジャーナルBritish Journal of Haematology
124
発行部数6
DOI
出版物ステータスPublished - 2004 3

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Idiopathic Thrombocytopenic Purpura
Single Nucleotide Polymorphism
Tumor Necrosis Factor-alpha
Cytokines
Genes
Phenotype
B-Lymphocytes
Platelet Membrane Glycoproteins
Antibody-Producing Cells
Platelet Glycoprotein GPIIb-IIIa Complex
HLA Antigens
Interleukin-1
Blood Cells
Alleles
Odds Ratio
Confidence Intervals

ASJC Scopus subject areas

  • Hematology

これを引用

Single nucleotide polymorphisms of the inflammatory cytokine genes in adults with chronic immune thrombocytopenic purpura. / Satoh, Takashi; Pandey, Janardan P.; Okazaki, Yuka; Yasuoka, Hidekata; Kawakami, Yutaka; Ikeda, Yasuo; Kuwana, Masataka.

:: British Journal of Haematology, 巻 124, 番号 6, 03.2004, p. 796-801.

研究成果: Article

Satoh, Takashi ; Pandey, Janardan P. ; Okazaki, Yuka ; Yasuoka, Hidekata ; Kawakami, Yutaka ; Ikeda, Yasuo ; Kuwana, Masataka. / Single nucleotide polymorphisms of the inflammatory cytokine genes in adults with chronic immune thrombocytopenic purpura. :: British Journal of Haematology. 2004 ; 巻 124, 番号 6. pp. 796-801.
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abstract = "Single nucleotide polymorphisms (SNPs) of inflammatory cytokine genes were examined in 84 adult Japanese patients with chronic immune thrombocytopenic purpura (ITP) and 56 race-matched healthy controls. The SNPs examined were within the genes encoding tumour necrosis factor (TNF)-α (-238 G/A and -308 G/A), TNF-β (+252 G/A), and interleukin (IL)-1β (-511 C/T and +3953 T/C). Of these SNPs, the frequency of the TNF-β (+252) G/G phenotype was significantly higher in ITP patients than in healthy controls (21{\%} vs. 7{\%}, P = 0.04, odds ratio = 3.6, 95{\%} confidence interval 1.1-11.1), while no significant association was detected for the other SNPs. The distribution of the TNF-β (+252) phenotype was not associated with human leucocyte antigen class II alleles or the therapeutic response in ITP patients. The frequency of circulating anti-glycoprotein IIb/IIIa antibody-producing B cells was significantly higher in ITP patients with the TNF-β (+252) G/G phenotype than in those with the G/A or A/A phenotype (11.9 ± 4.9 vs. 6.8 ± 4.9 and 3.7 ± 2.8 per 105 peripheral blood mononuclear cells; P = 0.02 and P < 0.001, respectively). These findings suggest that the SNP located at TNF-β (+252) contributes to susceptibility to chronic ITP by controlling the autoreactive B-cell responses to platelet membrane glycoproteins.",
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AU - Okazaki, Yuka

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AU - Kawakami, Yutaka

AU - Ikeda, Yasuo

AU - Kuwana, Masataka

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N2 - Single nucleotide polymorphisms (SNPs) of inflammatory cytokine genes were examined in 84 adult Japanese patients with chronic immune thrombocytopenic purpura (ITP) and 56 race-matched healthy controls. The SNPs examined were within the genes encoding tumour necrosis factor (TNF)-α (-238 G/A and -308 G/A), TNF-β (+252 G/A), and interleukin (IL)-1β (-511 C/T and +3953 T/C). Of these SNPs, the frequency of the TNF-β (+252) G/G phenotype was significantly higher in ITP patients than in healthy controls (21% vs. 7%, P = 0.04, odds ratio = 3.6, 95% confidence interval 1.1-11.1), while no significant association was detected for the other SNPs. The distribution of the TNF-β (+252) phenotype was not associated with human leucocyte antigen class II alleles or the therapeutic response in ITP patients. The frequency of circulating anti-glycoprotein IIb/IIIa antibody-producing B cells was significantly higher in ITP patients with the TNF-β (+252) G/G phenotype than in those with the G/A or A/A phenotype (11.9 ± 4.9 vs. 6.8 ± 4.9 and 3.7 ± 2.8 per 105 peripheral blood mononuclear cells; P = 0.02 and P < 0.001, respectively). These findings suggest that the SNP located at TNF-β (+252) contributes to susceptibility to chronic ITP by controlling the autoreactive B-cell responses to platelet membrane glycoproteins.

AB - Single nucleotide polymorphisms (SNPs) of inflammatory cytokine genes were examined in 84 adult Japanese patients with chronic immune thrombocytopenic purpura (ITP) and 56 race-matched healthy controls. The SNPs examined were within the genes encoding tumour necrosis factor (TNF)-α (-238 G/A and -308 G/A), TNF-β (+252 G/A), and interleukin (IL)-1β (-511 C/T and +3953 T/C). Of these SNPs, the frequency of the TNF-β (+252) G/G phenotype was significantly higher in ITP patients than in healthy controls (21% vs. 7%, P = 0.04, odds ratio = 3.6, 95% confidence interval 1.1-11.1), while no significant association was detected for the other SNPs. The distribution of the TNF-β (+252) phenotype was not associated with human leucocyte antigen class II alleles or the therapeutic response in ITP patients. The frequency of circulating anti-glycoprotein IIb/IIIa antibody-producing B cells was significantly higher in ITP patients with the TNF-β (+252) G/G phenotype than in those with the G/A or A/A phenotype (11.9 ± 4.9 vs. 6.8 ± 4.9 and 3.7 ± 2.8 per 105 peripheral blood mononuclear cells; P = 0.02 and P < 0.001, respectively). These findings suggest that the SNP located at TNF-β (+252) contributes to susceptibility to chronic ITP by controlling the autoreactive B-cell responses to platelet membrane glycoproteins.

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