| First Author | Dunkle A | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 3 | Pages | 940-7 |
| PubMed ID | 23269245 | Mgi Jnum | J:192594 |
| Mgi Id | MGI:5465474 | Doi | 10.4049/jimmunol.1103481 |
| Citation | Dunkle A, et al. (2013) Transfer of CD8+ T Cell Memory Using Bcl-2 as a Marker. J Immunol 190(3):940-7 |
| abstractText | The processes that regulate T cell memory generation are important for therapeutic design and the immune response to disease. However, what allows a subset of effector T cells to survive the contraction period to become memory cells is incompletely understood. The Bcl-2 family is critical for T cell survival, and Bcl-2 has been proposed to be important for the survival of memory cells. However, previous studies have relied on double-knockout models, potentially skewing the role of Bcl-2, and the use of Bcl-2 as a marker in adoptive transfer experiments, a method required to confirm the memory potential of cell subsets, has not been possible because of the intracellular localization of the protein. In this study, we present a novel Bcl-2 reporter mouse model and, to our knowledge, show for the first time that a distinct subset of effector T cells, and also a subset within the CD127(hi)KLRG1(lo) memory precursor effector cell population, retains high Bcl-2 expression at the peak of the CD8(+) T cell response to Listeria monocytogenes. Furthermore, we show that Bcl-2 correlates with memory potential in adoptive transfer experiments using both total responding CD8(+) T cells and memory precursor effector cells. These results show that even within the memory precursor effector cell population, Bcl-2 confers a survival advantage in a subset of effector CD8(+) T cells that allows differentiation into memory cells and cement Bcl-2 as a critical factor for T cell memory. |
