IndraLab
Statements
reach
"As the induction of Foxp3 by Tci-L4-ES is thought to be due to the presence of parasite homologues of transforming growth factor-beta (TGF-beta1), a cytokine which preferentially induces Foxp3 expression in naive rather than non naive CD4 + T cells [XREF_BIBR, XREF_BIBR], we also determined whether Tc-L4-ES was able to induce Foxp3 expression in purified naive ovine CD4 + T cells."
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"Thus, our data reveal that TGF-beta1 induces Foxp3 expression through at least two indispensable and interdependent molecular events : promoting E2A protein binding to the Foxp3 promoter (enhancer) and inhibiting and/or removing negative factors bound to the promoter such as GATA-3 (silencer)."
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"In this study, in vitro experiments were performed to determine whether TGF-beta1 could synergize with low-dose rapamycin and inhibit T cell activation and production of inflammatory cytokines, as well as enhance FoxP3 expression for potential application in islet transplantation."
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"Despite FoxP3 gene transcription by TGF-beta1 is vital mechanism of regulatory T cell stimulation [XREF_BIBR], recent findings showed that FoxP3 + regulatory cells, of potent anti-inflammatory activity, might be subgrouped based on the chemotactic receptor expression into different Th cell subsets, each functionally suppressive [XREF_BIBR]."
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"While TGF-beta1 is known to induce Foxp3 expression in CD4 T cells and may assist in the generation of peripheral Treg populations [XREF_BIBR], we did not observe an increase in the induction of Tregs in the scaffolds in either the blank or allogeneic transplantation models (XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY)."
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"In the present study, we investigated the involvement of NOTCH and TGF-beta 1 signaling pathways in regulating the FOXP3 transcription factor and demonstrated, for the first time, that FOXP3 expression was modulated by NOTCH and TGF-beta 1 pathways in primary and metastatic melanoma cell lines."
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"Based upon data presented here, we propose that TGF-beta1 induces Foxp3 expression through at least two indispensable and complementary molecular events : by promoting E protein binding to the Foxp3 promoter (enhancer) and by inhibiting and/or removing the negative factors bound to the Foxp3 promoter such as GATA-3 (silencer)."
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"In humans, neither forced Foxp3 overexpression XREF_BIBR nor Foxp3 expression triggered by TGF-beta1 alone XREF_BIBR results in the differentiation of suppressive Foxp3 + T reg cells, which indicates that additional signals beyond those controlled by Foxp3 are required for the generation of functional Foxp3 + T reg cells."