論文

査読有り
2017年5月

The cytokine polymorphisms affecting Th1/Th2 increase the susceptibility to, and severity of, chronic ITP

BMC IMMUNOLOGY
  • Noriyuki Takahashi
  • ,
  • Takayuki Saitoh
  • ,
  • Nanami Gotoh
  • ,
  • Yasuhiro Nitta
  • ,
  • Lobna Alkebsi
  • ,
  • Tetsuhiro Kasamatsu
  • ,
  • Yusuke Minato
  • ,
  • Akihiko Yokohama
  • ,
  • Norifumi Tsukamoto
  • ,
  • Hiroshi Handa
  • ,
  • Hirokazu Murakami

18
1
開始ページ
26
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1186/s12865-017-0210-3
出版者・発行元
BIOMED CENTRAL LTD

Background: T-helper cell type 1 (Th1) polarization in chronic immune thrombocytopenia (cITP) has been reported at the protein and mRNA levels. We evaluated the impact of Th1/Th2 cytokine and cytokine receptor functional polymorphisms on both susceptibility to, and severity of, cITP. We analysed IFN-gamma + 874 T/A, IFN-gamma R -611G/A, IL-4 -590C/T, and IL-4R alpha Q576R polymorphisms in 126 cITP patients (male/female: 34/92; median age: 47.7 years) and 202 healthy control donors. Genotyping was determined by PCR and direct sequencing. The Th1/Th2 ratio was detected in peripheral blood mononuclear cells via flow cytometry.
Results: cITP patients had a higher frequency of the IL-4R alpha 576 non-QQ genotype compared to healthy subjects (P = 0.04). cITP patients with the IFN-gamma + 874 non-AA genotype (high expression type) showed more severe thrombocytopenia than those with the AA genotype (P < 0.05). cITP patients had a significantly higher Th1/Th2 ratio than control patients (P < 0.01); this ratio was inversely correlated with platelet counts. Furthermore, patients with both IFN-gamma + 874 non-AA genotype (high expression type) and IFN-gamma R -611 non-AA genotype (high-function type) had a significantly higher Th1/Th2 ratio (P < 0.05).
Conclusions: The cytokine polymorphisms affecting Th1/Th2 increase the susceptibility to, and severity of, chronic ITP.

Web of Science ® 被引用回数 : 13

リンク情報
DOI
https://doi.org/10.1186/s12865-017-0210-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28511637
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000402364600001&DestApp=WOS_CPL