| First Author | Omilusik KD | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 3 | Pages | 773-783 |
| PubMed ID | 29440362 | Mgi Jnum | J:259228 |
| Mgi Id | MGI:6120127 | Doi | 10.1084/jem.20171584 |
| Citation | Omilusik KD, et al. (2018) Sustained Id2 regulation of E proteins is required for terminal differentiation of effector CD8(+) T cells. J Exp Med 215(3):773-783 |
| abstractText | CD8(+) T cells responding to infection differentiate into a heterogeneous population composed of progeny that are short-lived and participate in the immediate, acute response and those that provide long-lasting host protection. Although it is appreciated that distinct functional and phenotypic CD8(+) T cell subsets persist, it is unclear whether there is plasticity among subsets and what mechanisms maintain subset-specific differences. Here, we show that continued Id2 regulation of E-protein activity is required to maintain the KLRG1(hi) CD8(+) T cell population after lymphocytic choriomeningitis virus infection. Induced deletion of Id2 phenotypically and transcriptionally transformed the KLRG1(hi) "terminal" effector/effector-memory CD8(+) T cell population into a KLRG1(lo) memory-like population, promoting a gene-expression program that resembled that of central memory T cells. Our results question the idea that KLRG1(hi) CD8(+) T cells are necessarily terminally programmed and suggest that sustained regulation is required to maintain distinct CD8(+) T cell states. |
