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

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

研究成果: Contribution to journalArticle査読

9 被引用数 (Scopus)

抄録

Innate γδ T cells expressing Vγ6 produce IL-17A at an early stage following infection with Mycobacterium bovis Bacillus Calmette-Guérin (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 γδ T-cell response following BCG infection. IL-17A-producing Vγ6+ γδ 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 Vγ6+ γδ 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 Vγ6+ γδ T cells via Bim. Thus, these results suggest that IL-21 acts as a potent inhibitor of a IL-17A-producing γδ T-cell subset during BCG infection.

本文言語英語
ページ(範囲)588-597
ページ数10
ジャーナルInnate Immunity
22
8
DOI
出版ステータス出版済み - 11 1 2016

All Science Journal Classification (ASJC) codes

  • 微生物学
  • 免疫学
  • 分子生物学
  • 細胞生物学
  • 感染症

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