IL-21 inhibits IL-17A-producing γδ T-cell response after infection with Bacillus Calmette-Guérin via induction of apoptosis. Issue 8 (November 2016)

• Record Type: Journal Article
• Authors: Huang, Yinxia; Matsumura, Yumiko; Hatano, Shinya; Noguchi, Naoto; Murakami, Tesshin; Iwakura, Yoichiro; Sun, Xun; Ohara, Naoya; Yoshikai, Yasunobu
• Is Part Of: Innate immunity. Volume 22:Issue 8(2016:Nov.)
• Page Start: 588
• Page End: 597
• Publication Date: 2016-11
• Subjects: γδ T cells -- IL-21 -- IL-17A -- BCG -- apoptosis; Natural immunity -- Periodicals; Endotoxins -- Periodicals; 616.07905
• DOI: 10.1177/1753425916664125
• Languages: English
• ISSNs: 1753-4259

Abstract

Innate γδ T cells expressing Vγ6 produce IL-17A at an early stage following infection with Mycobacterium bovi s 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.