Cutting Edge: The Transcription Factor Eomesodermin Enables CD8+ T Cells To Compete for the Memory Cell Niche

被引:316
作者
Banerjee, Arnob [1 ,2 ]
Gordon, Scott M. [1 ,2 ]
Intlekofer, Andrew M. [1 ,2 ]
Paley, Michael A. [3 ]
Mooney, Erin C. [1 ,2 ]
Lindsten, Tulia [1 ,4 ]
Wherry, E. John [3 ]
Reiner, Steven L. [1 ,2 ]
机构
[1] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[2] Univ Penn, Dept Med, Philadelphia, PA 19104 USA
[3] Univ Penn, Dept Microbiol, Philadelphia, PA 19104 USA
[4] Univ Penn, Dept Pathol, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
BONE-MARROW; BET; EFFECTOR; DIFFERENTIATION; EXPRESSION; SUBSETS; SITE;
D O I
10.4049/jimmunol.1002042
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:4988 / 4992
页数:5
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