| http://purl.uniprot.org/citations/24586481 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24586481 | http://www.w3.org/2000/01/rdf-schema#comment | "Cytolytic CD4 T cells (CD4 CTL) have been identified in vivo in response to viral infections; however, the factors necessary for driving the cytolytic phenotype have not been fully elucidated. Our previously published work suggests IL-2 may be the master regulator of perforin-mediated cytotoxicity in CD4 effectors. To further dissect the role of IL-2 in CD4 CTL generation, T cell receptor transgenic mice deficient in the ability to produce IL-2 or the high affinity IL-2 receptor (IL-2Rα, CD25) were used. Increasing concentrations of IL-2 were necessary to drive perforin (Prf) expression and maximal cytotoxicity. Granzyme B (GrB) expression and killing correlated with STAT5 activation and CD25 expression in vitro, suggesting that signaling through the high affinity IL-2R is critical for full cytotoxicity. IL-2 signaling was also necessary in vivo for inducing the Th1 phenotype and IFN-γ expression in CD4 T cells during influenza A (IAV) infection. In addition, GrB expression, as measured by mean fluorescent intensity, was decreased in CD25 deficient cells; however, the frequency of CD4 cells expressing GrB was unchanged. Similarly, analysis of cytolytic markers such as CD107a/b and Eomesodermin indicate high IL-2Rα expression is not necessary to drive the CD4 CTL phenotype during IAV infection. Thus, inflammatory signals induced by viral infection may overcome the need for strong IL-2 signals in driving cytotoxicity in CD4 cells."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0089010"xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/author | "Brown D.M."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/author | "Jacobs A.K."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/author | "Condon S."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/author | "Workman A.M."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/author | "Vogel A.J."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/pages | "e89010"xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/title | "Inflammation enhances IL-2 driven differentiation of cytolytic CD4 T cells."xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://purl.uniprot.org/core/volume | "9"xsd:string |
| http://purl.uniprot.org/citations/24586481 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24586481 |
| http://purl.uniprot.org/citations/24586481 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24586481 |
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| http://purl.uniprot.org/uniprot/#_P04351-mappedCitation-24586481 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24586481 |
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