TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.
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Role of Autophagy and Apoptosis in the Postinfluenza Bacterial PneumoniaHighly pathogenic avian influenza H5N1 virus delays apoptotic responses via activation of STAT3.Exogenous Activation of Invariant Natural Killer T Cells by α-Galactosylceramide Reduces Pneumococcal Outgrowth and Dissemination PostinfluenzaInflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections.Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection.Influenza A Virus Infection Predisposes Hosts to Secondary Infection with Different Streptococcus pneumoniae Serotypes with Similar Outcome but Serotype-Specific Manifestation.Hierarchical effects of pro-inflammatory cytokines on the post-influenza susceptibility to pneumococcal coinfection.Type I Interferons as Regulators of Lung Inflammation.The Roles of Type I Interferon in Bacterial Infection.The inflammatory response triggered by Influenza virus: a two edged sword.Protection against Streptococcus pneumoniae Invasive Pathogenesis by a Protein-Based Vaccine Is Achieved by Suppression of Nasopharyngeal Bacterial Density during Influenza A Virus Coinfection.The Impact of the Interferon/TNF-Related Apoptosis-Inducing Ligand Signaling Axis on Disease Progression in Respiratory Viral Infection and Beyond.Influenza A virus-induced release of interleukin-10 inhibits the anti-microbial activities of invariant natural killer T cells during invasive pneumococcal superinfection.Influenza A virus infection impacts systemic microbiota dynamics and causes quantitative enteric dysbiosis.Cytokine-Ion Channel Interactions in Pulmonary Inflammation.Neutrophil extracellular traps in immunity and disease.The Murine Natural Cytotoxic Receptor NKp46/NCR1 Controls TRAIL Protein Expression in NK Cells and ILC1s.Interleukin-22 immunotherapy during severe influenza enhances lung tissue integrity and reduces secondary bacterial systemic invasion.Lethal Synergism between Influenza andTreating Influenza Infection, From Now and Into the FutureBack to the Future: Lessons Learned From the 1918 Influenza PandemicAlteration of Flt3-Ligand-dependent de novo generation of conventional dendritic cells during influenza infection contributes to respiratory bacterial superinfectionRole of Inflammatory Risk Factors in the Pathogenesis ofCoinfection With Influenza A Virus and : An Underrecognized Impact on Host Resistance and Tolerance to Pulmonary Infections
P2860
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P2860
TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@ast
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@en
type
label
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@ast
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@en
prefLabel
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@ast
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@en
P2093
P2860
P50
P356
P1433
P1476
TRAIL+ monocytes and monocyte- ...... coccus pneumoniae coinfection.
@en
P2093
Gregory T Ellis
Sophia Davidson
Venizelos Papayannopoulos
P2860
P304
P356
10.15252/EMBR.201540473
P577
2015-08-11T00:00:00Z