Cutting edge: The transcription factor eomesodermin enables CD8⁺ T cells to compete for the memory cell niche

CD8⁺ T cells responding to intracellular infection give rise to cellular progeny that become terminally differentiated effector cells and self-renewing memory cells. T-bet and eomesodermin (Eomes) are key transcription factors of cytotoxic lymphocyte lineages. We show in this study that CD8 ⁺ T cells lacking Eomes compete poorly in contributing to the pool of Ag-specific central memory cells. Eomes-deficient CD8⁺ T cells undergo primary clonal expansion but are defective in long-term survival, populating the bone marrow niche and reexpanding postrechallenge. The phenotype of Eomesdeficient CD8⁺ T cells supports the hypothesis that T-bet and Eomes can act redundantly to induce effector functions, but can also act to reciprocally promote terminal differentiation versus self-renewal of Ag-specific memory cells.