{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T14:18:56Z","timestamp":1777731536414,"version":"3.51.4"},"reference-count":45,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2016,9,22]],"date-time":"2016-09-22T00:00:00Z","timestamp":1474502400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Innate Immun"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:p>\n                    Innate \u03b3\u03b4 T cells expressing V\u03b36 produce IL-17A at an early stage following infection with Mycobacterium bovis Bacillus Calmette-Gu\u00e9rin (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 \u03b3\u03b4 T-cell response following BCG infection. IL-17A-producing V\u03b36\n                    <jats:sup>+<\/jats:sup>\n                    \u03b3\u03b4 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 V\u03b36\n                    <jats:sup>+<\/jats:sup>\n                    \u03b3\u03b4 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 V\u03b36\n                    <jats:sup>+<\/jats:sup>\n                    \u03b3\u03b4 T cells via Bim. Thus, these results suggest that IL-21 acts as a potent inhibitor of a IL-17A-producing \u03b3\u03b4 T-cell subset during BCG infection.\n                  <\/jats:p>","DOI":"10.1177\/1753425916664125","type":"journal-article","created":{"date-parts":[[2016,8,23]],"date-time":"2016-08-23T20:18:03Z","timestamp":1471983483000},"page":"588-597","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":17,"title":["IL-21 inhibits IL-17A-producing \u03b3\u03b4 T-cell response after infection with Bacillus Calmette-Gu\u00e9rin via induction of apoptosis"],"prefix":"10.1177","volume":"22","author":[{"given":"Yinxia","family":"Huang","sequence":"first","affiliation":[{"name":"Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan"},{"name":"Beijing Key Laboratory of Drug Resistance Tuberculosis, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Chest Hospital, Capital Medical 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