TRAIL limits excessive host immune responses in bacterial meningitis.
about
Pathophysiology and treatment of bacterial meningitisApoptosis is essential for neutrophil functional shutdown and determines tissue damage in experimental pneumococcal meningitisActivation of kinin receptor B1 limits encephalitogenic T lymphocyte recruitment to the central nervous systemTRAIL induces neutrophil apoptosis and dampens sepsis-induced organ injury in murine colon ascendens stent peritonitis.Airway Inflammation after Bronchial Thermoplasty for Severe Asthma.Soluble TRAIL in normal pregnancy and acute pyelonephritis: a potential explanation for the susceptibility of pregnant women to microbial products and infection.Polymorphisms in Toll-like receptors 2, 4, and 9 are highly associated with hearing loss in survivors of bacterial meningitis.Thrombopoietin contributes to neuronal damage in experimental bacterial meningitis.Bacterial pore-forming cytolysins induce neuronal damage in a rat model of neonatal meningitis.Pneumococcal meningitis and vaccine effects in the era of conjugate vaccination: results of 20 years of nationwide surveillance in GermanyTumor necrosis factor-related apoptosis-inducing ligand induces the expression of proinflammatory cytokines in macrophages and re-educates tumor-associated macrophages to an antitumor phenotypeTNF-related apoptosis-inducing ligand (TRAIL) exerts therapeutic efficacy for the treatment of pneumococcal pneumonia in mice.TNF-related apoptosis-inducing ligand (TRAIL) regulates inflammatory neutrophil apoptosis and enhances resolution of inflammation.Novel biphasic role for lymphocytes revealed during resolving inflammationTherapeutic applications of TRAIL receptor agonists in cancer and beyond.Following TRAIL's path in the immune system.Bacterial meningitis: current therapy and possible future treatment options.Pathways mediating resolution of inflammation: when enough is too much.Distinct roles of TNF-related apoptosis-inducing ligand (TRAIL) in viral and bacterial infections: from pathogenesis to pathogen clearance.Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced chemokine release in both TRAIL-resistant and TRAIL-sensitive cells via nuclear factor kappa B.CD8+ T cells use TRAIL to restrict West Nile virus pathogenesis by controlling infection in neurons.Lymphocytes modulate innate immune responses and neuronal damage in experimental meningitis.Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation.Microglia inflict delayed brain injury after subarachnoid hemorrhage.
P2860
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P2860
TRAIL limits excessive host immune responses in bacterial meningitis.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
TRAIL limits excessive host immune responses in bacterial meningitis.
@en
type
label
TRAIL limits excessive host immune responses in bacterial meningitis.
@en
prefLabel
TRAIL limits excessive host immune responses in bacterial meningitis.
@en
P2093
P2860
P50
P356
P1476
TRAIL limits excessive host immune responses in bacterial meningitis.
@en
P2093
Cordula Mahrhofer
Joerg R Weber
Nevena Baeva
Olaf Hoffmann
Orhan Aktas
Sarah Stricker
Timour Prozorovski
Ulf Schulze-Topphoff
P2860
P304
P356
10.1172/JCI30356
P407
P577
2007-07-01T00:00:00Z