期刊
NATURE IMMUNOLOGY
卷 9, 期 10, 页码 1140-1147出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1649
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资金
- Japan Society for the Promotion of Science
- Ministry of Education, Culture, Sports, Science and Technology
- Takeda Science Foundation
- Sumitomo Foundation
- Mochida Memorial Foundation
- Grants-in-Aid for Scientific Research [20679005] Funding Source: KAKEN
The acquisition of cytotoxic effector function by CD8(+) T cells is crucial for the control of intracellular infection and tumor invasion. However, it remains unclear which signaling pathways are required for the differentiation of CD8(+) cytotoxic T lymphocytes. We show here that Notch2-deficient T cells had impaired differentiation into cytotoxic T lymphocytes. In addition, dendritic cells with lower expression of the Notch ligand Delta-like 1 induced the differentiation of cytotoxic T lymphocytes less efficiently. We found that the intracellular domain of Notch2 interacted with a phosphorylated form of the transcription factor CREB1, and together these proteins bound the transcriptional coactivator p300 to form a complex on the promoter of the gene encoding granzyme B. Our results suggest that the highly regulated, dynamic control of T cell cytotoxicity depends on the integration of Notch2 and CREB1 signals.
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