Abstract
Abstract CD4+Foxp3+ regulatory T (Treg) cells are key players in preventing lethal autoimmunity and excessive inflammation. Based on their functional status, Treg cells can be distinguished into central (resting) and effector (activated) subsets. The homeostatic regulation between these two subsets is essential for Treg biology. However, what controls the dynamics between central and effector Treg cells remains poorly understood. We find that Wnt signaling transcription factor, TCF-1 plays a central role in regulating the differentiation from central to effector Treg cells. Although TCF-1 is crucial for T cell lineage specification, its expression is declined in a precisely-quantitative manner over the course of Treg development. Based on the expression of TCF-1, effector Treg cells can be further divided into two subsets. TCF-1neg subset is characterized as bona fide effector Treg cells. Transgenic modulation of TCF-1 alters the abundance of effector Treg cells. Our data suggest a two-step regulation of peripheral Treg homeostasis and TCF-1 play a critical role in this process.
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