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http://purl.uniprot.org/citations/28546549http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28546549http://www.w3.org/2000/01/rdf-schema#comment"Production of IFN-γ contributes to host defense against Mycobacterium tuberculosis (Mtb) infection. We previously demonstrated that Signaling lymphocytic activation molecule-associated protein (SAP) expression on cells from tuberculosis (TB) patients was inversely correlated with IFN-γ production. Here we first investigated the role of NK, T- and B-cell antigen (NTB-A)/SAP pathway in the regulation of Th1 response against Mtb. Upon antigen stimulation, NTB-A phosphorylation rapidly increases and afterwards modulates IFN-γ and IL-17 secretion. To sustain a healthy immune system, controlled expansion and contraction of lymphocytes, both during and after an adaptive immune response, is essential. Besides, restimulation-induced cell death (RICD) results in an essential homeostatic mechanism for precluding excess T-cell accumulation and associated immunopathology during the course of certain infections. Accordingly, we found that the NTB-A/SAP pathway was required for RICD during active tuberculosis. In low responder (LR) TB patients, impaired RICD was associated with diminished FASL levels, IL-2 production and CD25high expression after cell-restimulation. Interestingly, we next observed that SAP mediated the recruitment of the Src-related kinase FYNT, only in T cells from LR TB patients that were resistant to RICD. Together, we showed that the NTB-A/SAP pathway regulates T-cell activation and RICD during human TB. Moreover, the NTB-A/SAP/FYNT axis promotes polarization to an unfavorable Th2-phenotype."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.org/dc/terms/identifier"doi:10.1038/icb.2017.42"xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Garcia V.E."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Pena D."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Malbran A."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Musella R.M."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Pasquinelli V."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Rovetta A.I."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Palmero D.J."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Hernandez Del Pino R.E."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Pellegrini J.M."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Rolandelli A."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/author"Alvarez G.I."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/name"Immunol Cell Biol"xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/pages"716-728"xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/title"Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses."xsd:string
http://purl.uniprot.org/citations/28546549http://purl.uniprot.org/core/volume"95"xsd:string
http://purl.uniprot.org/citations/28546549http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28546549
http://purl.uniprot.org/citations/28546549http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28546549
http://purl.uniprot.org/uniprot/#_A0A8V8TLH8-mappedCitation-28546549http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28546549
http://purl.uniprot.org/uniprot/#_B4E1U5-mappedCitation-28546549http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28546549
http://purl.uniprot.org/uniprot/#_B7Z6A7-mappedCitation-28546549http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28546549
http://purl.uniprot.org/uniprot/#_K7YQB3-mappedCitation-28546549http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28546549