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

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)588-597
Number of pages10
JournalInnate Immunity
Volume22
Issue number8
DOIs
Publication statusPublished - Nov 1 2016

Keywords

  • BCG
  • IL-17A
  • IL-21
  • apoptosis
  • γδ T cells

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Molecular Biology
  • Cell Biology
  • Infectious Diseases

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