Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 9, Pages 4988-4992Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002042
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Funding
- National Institutes of Health [AI061699, AI076458, AI071309, AI007324, AI055428, CA076931, CA09140]
- Abramson Family Cancer Research Institute
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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. The Journal of Immunology, 2010, 185: 4988-4992.
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