http://purl.uniprot.org/citations/21742968 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/21742968 | http://www.w3.org/2000/01/rdf-schema#comment | "Defects in the Bcl-2-regulated apoptotic pathway inhibit the deletion of self-reactive T cells. What is unresolved, however, is the nature and fate of such self-reactive T cells escaping deletion. In this study, we report that mice with such defects contained increased numbers of CD25(low)Foxp3(+) cells in the thymus and peripheral lymph tissues. The increased CD25(low)Foxp3(+) population contained a large fraction of cells bearing self-reactive TCRs, evident from a prominent increase in self-superantigen-specific Foxp3(+)Vβ5(+)CD4(+) T cells in BALB/c Bim(-/-) mice compared with control animals. The survival rate of the expanded CD25(low)Foxp3(+) cells was similar to that of CD25(high)Foxp3(+) CD4 T cells in vitro and in vivo. IL-2R stimulation, but not TCR ligation, upregulated CD25 on CD25(low)Foxp3(+)CD4(+) T cells in vitro and in vivo. The expanded CD25(low)Foxp3(+)CD4(+) T cells from Bim(-/-) mice were anergic but also had weaker regulatory function than CD25(high)Foxp3(+) CD4(+) T cells from the same mice. Analysis of Bim(-/-) mice that also lacked Fas showed that the peripheral homeostasis of this expanded population was in part regulated by this death receptor. In conclusion, these results show that self-reactive T cell escapes from thymic deletion in mice defective in the Bcl-2-regulated apoptotic pathway upregulate Foxp3 and become unresponsive upon encountering self-Ag without necessarily gaining potent regulatory function. This clonal functional diversion may help to curtail autoaggressiveness of escaped self-reactive CD4(+) T cells and thereby safeguard immunological tolerance."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1100027"xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Zhan Y."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Lew A.M."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Ko H.J."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "O'Reilly L."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Bouillet P."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Strasser A."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Gray D."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Wicks I.P."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/author | "Carrington E.M."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/pages | "1566-1577"xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/title | "Defects in the Bcl-2-regulated apoptotic pathway lead to preferential increase of CD25 low Foxp3+ anergic CD4+ T cells."xsd:string |
http://purl.uniprot.org/citations/21742968 | http://purl.uniprot.org/core/volume | "187"xsd:string |
http://purl.uniprot.org/citations/21742968 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21742968 |
http://purl.uniprot.org/citations/21742968 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21742968 |
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