Critical roles of Bcl11b in T-cell development and maintenance of T-cell identity

被引:84
作者
Liu, Pentao [1 ]
Li, Peng [1 ]
Burke, Shannon [1 ]
机构
[1] Wellcome Trust Sanger Inst, Cambridge CB10 1HH, England
关键词
Bcl11b; T cells; transcription factor; identity; natural killer; reprogramming; immunotherapy; NATURAL-KILLER-CELLS; ACUTE LYMPHOBLASTIC-LEUKEMIA; TRANSCRIPTION FACTOR BCL11B; MOUSE THYMIC LYMPHOMAS; ZINC-FINGER PROTEIN; HELIX INHIBITOR ID2; IN-VIVO; GENE-EXPRESSION; ALPHA-BETA; THYMOCYTE DEVELOPMENT;
D O I
10.1111/j.1600-065X.2010.00953.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T-cell development primarily occurs in the thymus and involves in the interactions of many important transcription factors. Until recently, no single transcription factor has been identified to be essential for T-cell lineage commitment or maintenance of T-cell identity. Recent studies have now identified the zinc finger transcription factor Bcl11b to be essential for T-cell development and for maintenance of T-cell identity. Remarkably, T cells acquire NK cell properties upon Bcl11b deletion. These reprogrammed cells have unique properties in proliferation, cytokine dependency and killing target cells, and may therefore provide a new cell source for some cell-based therapies.
引用
收藏
页码:138 / 149
页数:12
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