| http://purl.uniprot.org/citations/22753932 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22753932 | http://www.w3.org/2000/01/rdf-schema#comment | "Activation of the transcription factor NF-κB is critical for cytokine production and T cell survival after TCR engagement. The effects of persistent NF-κB activity on T cell function and survival are poorly understood. In this study, using a murine model that expresses a constitutively active form of inhibitor of NF-κB kinase β (caIKKβ) in a T cell-specific manner, we demonstrate that chronic inhibitor of NF-κB kinase β signaling promotes T cell apoptosis, attenuates responsiveness to TCR-mediated stimulation in vitro, and impairs T cell responses to bacterial infection in vivo. caIKKβ T cells showed increased Fas ligand expression and caspase-8 activation, and blocking Fas/Fas ligand interactions enhanced cell survival. T cell unresponsiveness was associated with defects in TCR proximal signaling and elevated levels of B lymphocyte-induced maturation protein 1, a transcriptional repressor that promotes T cell exhaustion. caIKKβ T cells also showed a defect in IL-2 production, and addition of exogenous IL-2 enhanced their survival and proliferation. Conditional deletion of B lymphocyte-induced maturation protein 1 partially rescued the sensitivity of caIKKβ T cells to TCR triggering. Furthermore, adoptively transferred caIKKβ T cells showed diminished expansion and increased contraction in response to infection with Listeria monocytogenes expressing a cognate Ag. Despite their functional defects, caIKKβ T cells readily produced proinflammatory cytokines, and mice developed autoimmunity. In contrast to NF-κB's critical role in T cell activation and survival, our study demonstrates that persistent IKK-NF-κB signaling is sufficient to impair both T cell function and survival."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1102429"xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Gao J."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Shin J."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Xie D."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Krishna S."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Zhong X.P."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/author | "Gorentla B."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/pages | "1209-1219"xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/title | "Chronic activation of the kinase IKKbeta impairs T cell function and survival."xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://purl.uniprot.org/core/volume | "189"xsd:string |
| http://purl.uniprot.org/citations/22753932 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22753932 |
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