| http://purl.uniprot.org/citations/24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24165986 | http://www.w3.org/2000/01/rdf-schema#comment | "The generation of CD4⁺Foxp3⁺ Treg cells in the thymus is crucial for immune homeostasis and self-tolerance. Recent studies have shown Treg-cell plasticity when Th-related transcriptional factors and cytokines are present. However, the mechanisms that maintain the stability of Treg cells are poorly understood. Here, using mice with a T-cell-specific deletion of the transforming growth factor-β receptor 2 (Tgfbr2⁻/⁻ mice), we identify the restriction of AKT activation as a key event for the control of Treg-cell stability in Th1 inflammation. AKT regulation was evident in thymic CD4⁺Foxp3⁺ Treg cells before they egressed to peripheral tissues. CD4⁺Foxp3⁺ thymocytes from mice with the Tgfbr2 deletion expressed high levels of CXCR3 and T-bet, and produced IFN-γ and TNF-α. Thymic Tgfbr2⁻/⁻ Treg cells also showed an increase in the activation of AKT pathway. Enhanced AKT activity induced the expression of IFN-γ both in natural and inducible Treg cells. Inhibition of AKT activity markedly attenuated the expression of IFN-γ and TNF-α in thymic Tgfbr2⁻/⁻ Treg cells in vivo. In addition, mixed bone marrow transplantation showed that TGF-β signaling maintained Treg-cell stability in an intrinsic manner. Our results demonstrate that AKT hyperactivation contributes to the conversion of Treg cells to a Th1 phenotype."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.org/dc/terms/identifier | "doi:10.1002/eji.201243291"xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Liu Y.'"xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Sun J."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Zhang F."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Xu Y."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Xu G."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Xia S."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/author | "Ma A."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/name | "Eur J Immunol"xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/pages | "521-532"xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/title | "AKT hyperactivation confers a Th1 phenotype in thymic Treg cells deficient in TGF-beta receptor II signaling."xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://purl.uniprot.org/core/volume | "44"xsd:string |
| http://purl.uniprot.org/citations/24165986 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24165986 |
| http://purl.uniprot.org/citations/24165986 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24165986 |
| http://purl.uniprot.org/uniprot/#_D3Z783-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_D3YYP9-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_D3YXX3-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_A4FUQ9-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_Q62312-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_Q3UG22-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |
| http://purl.uniprot.org/uniprot/#_Q8BQS9-mappedCitation-24165986 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24165986 |