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BATF3 programs CD8+T cell memory
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DOI：10.1038/s41590-020-0786-2.png)
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Abstract
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BATF3 is a member of the AP-1 transcription factor family. Kastenmuller and colleagues show that BATF3 is needed to promote memory CD8(+)T cell responses. Activated CD8(+)T cells transiently upregulate BATF3, which in turn suppresses expression of proapoptotic BIM to promote cell survival. Antiviral CD8(+)T cell responses are characterized by an initial activation/priming of T lymphocytes followed by a massive proliferation, subset differentiation, population contraction and the development of a stable memory pool. The transcription factor BATF3 has been shown to play a central role in the development of conventional dendritic cells, which in turn are critical for optimal priming of CD8(+)T cells. Here we show that BATF3 was expressed transiently within the first days after T cell priming and had long-lasting T cell-intrinsic effects. T cells that lackedBatf3showed normal expansion and differentiation, yet succumbed to an aggravated contraction and had a diminished memory response. Vice versa, BATF3 overexpression in CD8(+)T cells promoted their survival and transition to memory. Mechanistically, BATF3 regulated T cell apoptosis and longevity via the proapoptotic factor BIM. By programing CD8(+)T cell survival and memory, BATF3 is a promising molecule to optimize adoptive T cell therapy in patients.
Keywords:
TRANSCRIPTION FACTOR
T-CELLS
DENDRITIC CELLS
CHEMOKINE RECEPTOR
EFFECTOR
AP-1
SUBSETS
ROLES
DIFFERENTIATION
IDENTIFICATION
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