TY - JOUR
T1 - IL-21 inhibits IL-17A-producing γδ T-cell response after infection with Bacillus Calmette-Guérin via induction of apoptosis
AU - Huang, Yinxia
AU - Matsumura, Yumiko
AU - Hatano, Shinya
AU - Noguchi, Naoto
AU - Murakami, Tesshin
AU - Iwakura, Yoichiro
AU - Sun, Xun
AU - Ohara, Naoya
AU - Yoshikai, Yasunobu
N1 - Funding Information:
This work was supported by Grants-in-Aid (25670213; 26293098) from the Japan Society for the Promotion of Science, Yakult Bioscience Foundation (Y.Y.), and the Takeda Science Foundation (Y.Y.).
Publisher Copyright:
© SAGE Publications.
PY - 2016/11/1
Y1 - 2016/11/1
N2 - 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.
AB - 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.
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U2 - 10.1177/1753425916664125
DO - 10.1177/1753425916664125
M3 - Article
C2 - 27554052
AN - SCOPUS:84992049111
VL - 22
SP - 588
EP - 597
JO - Journal of Endotoxin Research
JF - Journal of Endotoxin Research
SN - 1753-4259
IS - 8
ER -
