期刊
IMMUNOLOGICAL REVIEWS
卷 238, 期 -, 页码 150-168出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1600-065X.2010.00964.x
关键词
hematopoietic progenitor cells; T cells; transcription factors; cell differentiation; gene regulation; lineage commitment; specification
类别
资金
- California Institute for Regenerative Medicine
- NIH [RC2 CA148278, R33 HL089123, R01 CA90233]
- Caltech-City of Hope Biomedical Initiative
- Louis Garfinkle Memorial Laboratory
- Al Sherman Foundation
T-cell development from stem cells has provided a highly accessible and detailed view of the regulatory processes that can go into the choice of a cell fate in a postembryonic, stem cell-based system. But it has been a view from the outside. The problems in understanding the regulatory basis for this lineage choice begin with the fact that too many transcription factors are needed to provide crucial input: without any one of them, T-cell development fails. Furthermore, almost all the factors known to provide crucial functions during the climax of T-lineage commitment itself are also vital for earlier functions that establish the pool of multilineage precursors that would normally feed into the T-cell specification process. When the regulatory genes that encode them are mutated, the confounding effects on earlier stages make it difficult to dissect T-cell specification genetically. Yet both the positive and the negative regulatory events involved in the choice of a T-cell fate are actually a mosaic of distinct functions. New evidence has emerged recently that finally provides a way to separate the major components that fit together to drive this process. Here, we review insights into T-cell specification and commitment that emerge from a combination of molecular, cellular, and systems biology approaches. The results reveal the regulatory structure underlying this lineage decision.
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