論文

査読有り
2016年11月

IL-21 inhibits IL-17A-producing T-cell response after infection with Bacillus Calmette-Guerin via induction of apoptosis

INNATE IMMUNITY
  • Yinxia Huang
  • ,
  • Yumiko Matsumura
  • ,
  • Shinya Hatano
  • ,
  • Naoto Noguchi
  • ,
  • Tesshin Murakami
  • ,
  • Yoichiro Iwakura
  • ,
  • Xun Sun
  • ,
  • Naoya Ohara
  • ,
  • Yasunobu Yoshikai

22
8
開始ページ
588
終了ページ
597
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1177/1753425916664125
出版者・発行元
SAGE PUBLICATIONS LTD

Innate T cells expressing V6 produce IL-17A at an early stage following infection with Mycobacterium bovis Bacillus Calmette-Guerin (BCG). In this study, we used IL-21 receptor knockout (IL-21R KO) mice and IL-21-producing recombinant BCG mice (rBCG-Ag85B-IL-21) to examine the role of IL-21 in the regulation of IL-17A-producing innate T-cell response following BCG infection. IL-17A-producing V6(+) T cells increased in the peritoneal cavity of IL-21R KO mice more than in wild type mice after BCG infection. In contrast, the number of IL-17A-producing V6(+) T cells was significantly lower after inoculation with rBCG-Ag85B-IL-21 compared with control rBCG-Ag85B. Notably, exogenous IL-21 selectively induced apoptosis of IL-17A-producing V6(+) T cells via Bim. Thus, these results suggest that IL-21 acts as a potent inhibitor of a IL-17A-producing T-cell subset during BCG infection.

Web of Science ® 被引用回数 : 9

リンク情報
DOI
https://doi.org/10.1177/1753425916664125
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27554052
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000386853400002&DestApp=WOS_CPL

エクスポート
BibTeX RIS