Maintenance of the Foxp3-dependent developmental program in mature regulatory T cells requires continued expression of Foxp3

By L. Williams, Alexander Y. Rudensky. Nature Immunology, 2007

910 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/04a449746d117b9848daea3f3feb2d9b27a784e2

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In Immunology

Citations in the corpus

Molecular antagonism and plasticity of regulatory and inflammatory T cell programs. (2008, background): “…observed that deletion of the Foxp3 gene in mature nTreg cells resulted in loss of suppressive function and upregulation of IL-17 and IL-21 expression (Williams and Rudensky, 2007), suggesting that the suppression of Th17 gene expression and the maintenance of Treg programs both require Foxp3.”
Regulatory T cells expressing interleukin 10 develop from Foxp3+ and Foxp3− precursor cells in the absence of interleukin 10 (2007, background): “Foxp3 initiates and supports a program of gene expression that specifies the development and maintenance of this lineag”
Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression (2007, background): “Moreover, the deletion of Foxp3 results in the reduced expression of such putative suppressor genes ( 17 ).”
T-bet controls regulatory T cell homeostasis and function during type-1 inflammation (2009, background): “In addition, loss of T reg cells results in uncontrolled T H 1 responses, which further demonstrates the important and nonredundant function of T reg cells in dampening type 1 inflammatio”
Regulatory T Cells and Foxp3 (2011, background): “Indeed, the ‘ex-Treg’ cells, upon transfer into lymphopenic recipients without functional Treg cells, caused severe tissue lesions and wasting disease (42).”
Foxp3 transcription-factor-dependent and -independent regulation of the regulatory T cell transcriptional signature. (2007, background): “…of the Treg cell lineage (including transcriptional activity at the Foxp3 locus) can be selected and persist in vivo in its absence (Gavin et al., 2007; Williams and Rudensky, 2007; Lin et al., 2007), consistent with the existence of Treg-like cells in some IPEX patients (Bacchetta et al., 2006).”
Function of miR-146a in controlling Treg cell-mediated regulation of Th1 responses (2010, positive): “Loss of Foxp3 in Treg cells resulted in the acquisition of the ability to produce proinflammatory cytokines, and cause tissue lesions in the absence of functional Treg cells (Williams and Rudensky, 2007; Zhou et al., 2009).”