期刊
CELL REPORTS
卷 13, 期 6, 页码 1118-1124出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.09.069
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资金
- BloodCenter Research Foundation
- American Cancer Society [86-004-26]
- Women's Health Research Program WHRP
- NIH [AI049360, AI109962, HL44612, AI079087]
- [NIGMST32-GM080202]
Control of chronic viral infections by CD8 T cells is critically dependent on CD4 help. In particular, helper- derived IL-21 plays a key role in sustaining the CD8 T cell response; however, the molecular pathways by which IL-21 sustains CD8 T cell immunity remain unclear. We demonstrate that IL-21 causes a phenotypic switch of transcription factor expression in CD8 T cells during chronic viral infection characterized by sustained BATF expression. Importantly, BATF expression during chronic infection is both required for optimal CD8 T cell persistence and anti-viral effector function and sufficient to rescue unhelped CD8 T cells. Mechanistically, BATF sustains the response by cooperating with IRF4, an antigen-induced transcription factor that is also critically required for CD8 T cell maintenance, to preserve Blimp-1 expression and thereby sustain CD8 T cell effector function. Collectively, these data suggest that CD4 T cells help the CD8 response during chronic infection via IL-21-induced BATF expression.
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