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10.1038/icb.2017.42 http://scihub22266oqcxt.onion/10.1038/icb.2017.42 C5595630!5595630 !28546549     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28546549 &cmd=llinks): Failed to open stream: HTTP request failed! 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Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses |pdf=|usr=}}{{28546549 }} gab.com Text Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses JO: Immunol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28546549 #FOAvip Production of IFN-? 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-? 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-? 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 CD25(high) 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. Twit Text FOAVip Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses ????Immunol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28546549 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28546549 #FOAvip English Wikipedia <ref>{{Cite pmid|28546549 }}</ref> Restimulation-induced T-cell death through NTB-A/SAP signaling pathway is impaired in tuberculosis patients with depressed immune responses #MMPMID28546549 Hernández Del Pino RE ; Pellegrini JM ; Rovetta AI ; Peña D ; Álvarez GI ; Rolandelli A ; Musella RM ; Palmero DJ ; Malbran A ; Pasquinelli V ; García VE Immunol Cell Biol 2017[Sep]; 95 (8 ): 716-728 PMID28546549 show ga Production of IFN-? 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-? 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-? 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 CD25(high) 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. |Adult [MESH] |Cell Death [MESH] |Cell Differentiation [MESH] |Cells, Cultured [MESH] |Female [MESH] |Homeostasis [MESH] |Humans [MESH] |Immunity [MESH] |Immunosuppression Therapy [MESH] |Interferon-gamma/metabolism [MESH] |Interleukin-17/metabolism [MESH] |Lymphocyte Activation [MESH] |Male [MESH] |Mycobacterium tuberculosis/*immunology [MESH] |Neoplasm Proteins/metabolism [MESH] |Protein-Tyrosine Kinases/metabolism [MESH] |Signal Transduction [MESH] |Signaling Lymphocytic Activation Molecule Family/*metabolism [MESH] |Th2 Cells/*immunology [MESH]Restimulation-induced T-cell death through NTB-A/SAP signaling pathway(epmc).pdf DeepDyve Pubget Overpricing