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

Arnob Banerjee, Scott M. Gordon, Andrew M. Intlekofer, Michael A. Paley, Erin C. Mooney, Tulia Lindsten, E. John Wherry, Steven L. Reiner

Research output: Contribution to journalArticlepeer-review

275 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)4988-4992
Number of pages5
JournalJournal of Immunology
Volume185
Issue number9
DOIs
StatePublished - Nov 1 2010

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