Graded levels of IRF4 regulate CD8+ T cell differentiation and expansion, but not attrition, in response to acute virus infection.

ABSTRACT: In response to acute virus infections, CD8(+) T cells differentiate to form a large population of short-lived effectors and a stable pool of long-lived memory cells. The characteristics of the CD8(+) T cell response are influenced by TCR affinity, Ag dose, and the inflammatory cytokine milieu dictated by the infection. To address the mechanism by which differences in TCR signal strength could regulate CD8(+) T cell differentiation, we investigated the transcription factor, IFN regulatory factor 4 (IRF4). We show that IRF4 is transiently upregulated to differing levels in murine CD8(+) T cells, based on the strength of TCR signaling. In turn, IRF4 controls the magnitude of the CD8(+) T cell response to acute virus infection in a dose-dependent manner. Modest differences in IRF4 expression d

SUBMITTER: Nayar R 

PROVIDER: S-EPMC4080788 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature