期刊
JOURNAL OF IMMUNOLOGY
卷 203, 期 2, 页码 323-327出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1900014
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资金
- National Key Research and Development Program [2016YFA0502203, 2016YFA0502204]
- National Natural Science Foundation of China [31770949, 31470870, 31770973, 31600709, 31770972]
- Chongqing Basic and Frontier Research Project [cstc2015jcyjBX0086]
The differentiation of memory CD8(+) T cells is critical to the long-term cellular immunity. The transcription factor BCL6 has been reportedly important for the generation and maintenance of memory CD8(+) T cells; however, using the newly established BCL6 conditional knockout mouse model, we demonstrate that BCL6 is dispensable for the maintenance of established memory CD8(+) T cell pool, although BCL6 is still required for the generation of CD8(+) memory precursors upon acute viral infection. In addition, BCL6 promotes the expression of TCF-1 via directly binding to the Tcf7 (gene symbol for TCF-1) allele in CD8(+) memory precursors and forced expression of TCF-1 restores the generation of BCL6-deficient memory precursors. Thus, our findings clarify that BCL6 is dispensable for the maintenance of memory CD8(+) T cells, but functions as an important upstream of TCF-1 to regulate the generation of memory precursors in acute viral infection.
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