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

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 re-expanding postrechallenge. The phenotype of Eomes-deficient 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.

SUBMITTER: Banerjee A

PROVIDER: S-EPMC2975552 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature

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

Banerjee Arnob A Gordon Scott M SM Intlekofer Andrew M AM Paley Michael A MA Mooney Erin C EC Lindsten Tulia T Wherry E John EJ Reiner Steven L SL

Journal of immunology (Baltimore, Md. : 1950) 20101008 9

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 surviv ...[more]

PMID: 20935204

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