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 (gene symbol for TCF-1) allele in CD8 memory precursors and forced expression of TCF-1 restores the generation of BCL6-deficient memory precursor... More
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 (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.