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http://purl.uniprot.org/citations/14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14688105http://www.w3.org/2000/01/rdf-schema#comment"We demonstrated previously that Actinobacillus actinomycetemcomitans leukotoxin (Ltx) is greatly able to induce apoptotic signaling in cells that are positive for lymphocyte function-associated antigen 1 (LFA-1), a cell receptor of Ltx. We investigated in this study whether inflammatory cytokines can regulate apoptosis of human leukemic HL-60 cells induced by Ltx. Of the cytokines tested, tumor necrosis factor alpha (TNF-alpha) significantly enhanced the Ltx-induced cell apoptosis. Northern and Western blotting analyses showed that TNF-alpha enhanced the expression of CD11a in the cells at both the mRNA and protein levels but did not do so for CD18 expression. TNF-alpha also enhanced the binding of Ltx to the cells. We also observed by measuring the mitochondrial transmembrane potential and the generation of superoxide anion that the cytokine enhanced Ltx-induced apoptosis in HL-60 cells. In addition, interleukin-1beta significantly enhanced Ltx-induced cell apoptosis, although the enhancing activity was lower than that of TNF-alpha. These stimulatory effects of both cytokines were also observed for human polymorphonuclear leukocytes. The ability of TNF-alpha to increase cell susceptibility to Ltx could be inhibited by preincubation of the cells with a monoclonal antibody against TNF receptor 1 but not by preincubation of the cells with a monoclonal antibody against anti-TNF receptor 2. Furthermore, the results of an assay of caspase 3 intracellular activity (PhiPhiLuxG1D2) showed that Ltx-induced caspase 3 activation was completely neutralized by CD18 antibody treatment, although significant neutralization was also observed with anti-CD11a antibody. Taken together, the results of the present study indicate that TNF-alpha acts as a potent stimulator of Ltx-induced HL-60 cell apoptosis via TNF receptor 1-mediated upregulation of LFA-1 expression."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.org/dc/terms/identifier"doi:10.1128/iai.72.1.269-276.2004"xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Kubo C."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Koga T."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Yamaguchi N."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Lally E.T."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Masuhiro Y."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/author"Hanazawa S."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/name"Infect Immun"xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/pages"269-276"xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/title"Tumor necrosis factor alpha enhances Actinobacillus actinomycetemcomitans leukotoxin-induced HL-60 cell apoptosis by stimulating lymphocyte function-associated antigen 1 expression."xsd:string
http://purl.uniprot.org/citations/14688105http://purl.uniprot.org/core/volume"72"xsd:string
http://purl.uniprot.org/citations/14688105http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/14688105
http://purl.uniprot.org/citations/14688105http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/14688105
http://purl.uniprot.org/uniprot/#_A0A0G2YPN5-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_A0A1U9X8M9-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_A0A411D318-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_A0A510GFL8-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_C1K3N5-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_B5BUQ6-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_A0A977WMN2-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_B2RAL6-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105
http://purl.uniprot.org/uniprot/#_B4DQ77-mappedCitation-14688105http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14688105