IL-2 regulates FOXP3 expression in human CD4+CD25+ regulatory T cells through a STAT-dependent mechanism and induces the expansion of these cells in vivo.

By E. Zorn, E. Nelson, M. Mohseni, F. Porcheray, Haesook T. Kim, Despina Litsa, R. Bellucci, E. Raderschall, C. Canning, R. Soiffer and 2 more. Blood, 2006

780 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9578bfb347c2c3531e6625f6ed9392c2914d5e05

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Citations in the corpus

CREB/ATF-dependent T cell receptor–induced FoxP3 gene expression: a role for DNA methylation (2007, methodology): “Consistent with previous observations (18, 19), using the VISTA computer program, we identifi ed three CNSs with >75% sequence identity between humans and mice.”
IL-2 Receptor β-Dependent STAT5 Activation Is Required for the Development of Foxp3+ Regulatory T Cells1 (2007, background): “(38) has also suggested that STAT5 regulates foxp3 expression, although they suggested that the relevant binding sites are those found within the first intron of the foxp3 gene.”
Functional delineation and differentiation dynamics of human CD4+ T cells expressing the FoxP3 transcription factor. (2009, background): “The 50 flanking region and a STAT5-responsive region in the in- tron 1 of the FOXP3 gene are critical for induction and enhance- ment of FoxP3 expression by TCR and IL-2 stimulation (Floess et al., 2007; Mantel et al., 2006; Zorn et al., 2006).”
Rapamycin Promotes Expansion of Functional CD4+CD25+FOXP3+ Regulatory T Cells of Both Healthy Subjects and Type 1 Diabetic Patients1 (2006, background): “(31) recently demonstrated that the IL-2-mediated up-regulation of FOXP3 in purified CD4 CD25 T cells involves the binding of STAT3/5 proteins to a highly conserved STAT binding site located in the first intron of the FOXP3 gene.”
Epigenetic Control of the foxp3 Locus in Regulatory T Cells (2007, result): “Tregs. This view is supported by recent findings with human natural killer (NK) cells, which up-regulated FOXP3 expression in response to IL-2 only after treatment with the demethylating agent 5-aza-2′deoxycytidine, demonstrating that this gene was constitutively repressed in non-Tregs by a mechanis”
IL-2 Is Essential for TGF-β to Convert Naive CD4+CD25− Cells to CD25+Foxp3+ Regulatory T Cells and for Expansion of These Cells1 (2007, background): “(43) reported that IL-2 selectively up-regulates the expression of Foxp3 in purified CD4 CD25 T cells but not in CD4 CD25 cells, the results of the present experiments suggest that the tolerizing effects of IL-2 on peripheral T cells are indirect.”
Interleukin-2 Receptor Signaling: At the Interface between Tolerance and Immunity (2010, unknown): “…in part is due to direct regulation of Foxp3 158 Immunity 33, August 27, 2010 ª2010 Elsevier Inc. and CD25 expression through Stat5 binding to respective enhancer elements of these genes (Yao et al., 2007; Zorn et al., 2006) to influence growth and survival signaling by the maturing Treg cells.”
The development of inflammatory TH-17 cells requires interferon-regulatory factor 4 (2007, background): “A binding site for STAT3 has been described in one intron of Foxp3 ; however, transfection assays have shown that binding of STAT3 to this site activates rather than suppresses Foxp3 expressio”
Nonredundant roles for Stat5a/b in directly regulating Foxp3. (2007, background): “Because of its role in binding IL-2, CD25 is a critical factor in regulating Foxp3.”
JAK and STAT signaling molecules in immunoregulation and immune-mediated disease. (2012, background): “Their effect is very direct in that STAT5A and STAT5B directly bind the Foxp3 gene and drive expression of this key gene (Yao et al., 2006, 2007; Zorn et al., 2006).”