Sustained Id2 regulation of E proteins is required for terminal differentiation of effector CD8⁺ T cells.

ABSTRACT: 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<

SUBMITTER: Omilusik KD 

PROVIDER: S-EPMC5839762 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature