High viral burden restricts short-lived effector cell number at late times postinfection through increased natural regulatory T cell expansion.
Ontology highlight
ABSTRACT: Generating and maintaining a robust CD8(+) T cell response in the face of high viral burden is vital for host survival. Further, balancing the differentiation of effectors along the memory precursor effector cell pathway versus the short-lived effector cell (SLEC) pathway may be critical in controlling the outcome of virus infection with regard to clearance and establishing protection. Although recent studies have identified several factors that have the capacity to regulate effector CD8(+) T cell differentiation-for example, inflammatory cytokines-we are far from a complete understanding of how cells choose the memory precursor effector cell versus SLEC fate following infection. In this study, we have modulated the infectious dose of the poxvirus vaccinia virus as an approach to modulate
SUBMITTER: Amoah S
PROVIDER: S-EPMC3711656 | biostudies-literature | 2013 May
REPOSITORIES: biostudies-literature
ACCESS DATA