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10.1086/500954

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16518756!7109654!16518756
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suck abstract from ncbi


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pmid16518756      J+Infect+Dis 2006 ; 193 (7): 945-53
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  • Functional tumor necrosis factor-related apoptosis-inducing ligand production by avian influenza virus-infected macrophages #MMPMID16518756
  • Zhou J; Law HK; Cheung CY; Ng IH; Peiris JS; Lau YL
  • J Infect Dis 2006[Apr]; 193 (7): 945-53 PMID16518756show ga
  • Severe human disease associated with influenza A H5N1 virus was first detected in Hong Kong in 1997. Its recent reemergence in Asia and high associated mortality highlight the need to understand its pathogenesis. We investigated the roles of death receptor ligands (DRLs) in H5N1 infection. Significant up-regulation of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and TNF-alpha, but not Fas ligand (FasL) mRNA, was detected in human monocyte-derived macrophages (MDMs) infected with avian influenza viruses A/Hong Kong/483/97 (H5N1/97) or its precursor, A/Quail/Hong Kong/G1/97. H5N1/97-infected MDMs exhibited the strongest induction of apoptosis in Jurkat T cells, and it could be reduced by TRAIL-receptor 2 blocking antibody. Furthermore, influenza virus infection enhanced the sensitivity of Jurkat T cells to apoptosis induced by TNF-alpha, TRAIL, and FasL. Our data suggested that functional TRAIL produced by influenza virus-infected MDMs was related to their cytotoxicity and that the enhanced sensitization to DRL-induced apoptosis detected in avian influenza may contribute to disease pathogenesis.
  • |*Apoptosis[MESH]
  • |Apoptosis Regulatory Proteins/*biosynthesis/genetics[MESH]
  • |Caspase 3[MESH]
  • |Caspases/analysis[MESH]
  • |Fas Ligand Protein[MESH]
  • |Gene Expression[MESH]
  • |Humans[MESH]
  • |Influenza A Virus, H5N1 Subtype/*pathogenicity[MESH]
  • |Jurkat Cells[MESH]
  • |Macrophages/*virology[MESH]
  • |Membrane Glycoproteins/*biosynthesis/genetics[MESH]
  • |RNA, Messenger/analysis[MESH]
  • |Receptors, TNF-Related Apoptosis-Inducing Ligand[MESH]
  • |Receptors, Tumor Necrosis Factor/antagonists & inhibitors[MESH]
  • |T-Lymphocytes/*cytology[MESH]
  • |TNF-Related Apoptosis-Inducing Ligand[MESH]
  • |Tumor Necrosis Factor-alpha/*biosynthesis/genetics[MESH]


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