| First Author | Ataide MA | Year | 2020 |
| Journal | Nat Immunol | Volume | 21 |
| Issue | 11 | Pages | 1397-1407 |
| PubMed ID | 32989328 | Mgi Jnum | J:306003 |
| Mgi Id | MGI:6706613 | Doi | 10.1038/s41590-020-0786-2 |
| Citation | Ataide MA, et al. (2020) BATF3 programs CD8(+) T cell memory. Nat Immunol 21(11):1397-1407 |
| abstractText | 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 lacked Batf3 showed 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. |
