Francisella tularensis live vaccine strain induces macrophage alternative activation as a survival mechanism.
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Abscisic acid regulates inflammation via ligand-binding domain-independent activation of peroxisome proliferator-activated receptor gammaExploring the full spectrum of macrophage activationThe role of macrophages and dendritic cells in the initiation of inflammation in IBDSubversion of host recognition and defense systems by Francisella sppTH1/TH2 paradigm extended: macrophage polarization as an unappreciated pathogen-driven escape mechanism?Protective and pathogenic functions of macrophage subsetsMacrophage activation and polarization: nomenclature and experimental guidelinesLive attenuated tularemia vaccines: recent developments and future goals.Monophosphoryl Lipid A Enhances Efficacy of a Francisella tularensis LVS-Catanionic Nanoparticle Subunit Vaccine against F. tularensis Schu S4 Challenge by Augmenting both Humoral and Cellular Immunity.Novel catanionic surfactant vesicle vaccines protect against Francisella tularensis LVS and confer significant partial protection against F. tularensis Schu S4 strainRole of TLR signaling in Francisella tularensis-LPS-induced, antibody-mediated protection against Francisella tularensis challenge.Microbial manipulation of receptor crosstalk in innate immunityIL-4 attenuates Th1-associated chemokine expression and Th1 trafficking to inflamed tissues and limits pathogen clearance.Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection.Pulmonary infection with an interferon-gamma-producing Cryptococcus neoformans strain results in classical macrophage activation and protection.An association between pulmonary Mycobacterium avium-intracellulare complex infections and biomarkers of Th2-type inflammation.Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signalingRole of methionine sulfoxide reductases A and B of Enterococcus faecalis in oxidative stress and virulenceGeneration of a convalescent model of virulent Francisella tularensis infection for assessment of host requirements for survival of tularemiaHost-pathogen interactions and immune evasion strategies in Francisella tularensis pathogenicityAgents that increase AAM differentiation blunt RSV-mediated lung pathology.IKKβ in myeloid cells controls the host response to lethal and sublethal Francisella tularensis LVS infection.Mast cell/IL-4 control of Francisella tularensis replication and host cell death is associated with increased ATP production and phagosomal acidificationMacrophages as IL-25/IL-33-responsive cells play an important role in the induction of type 2 immunity.Intracellular survival and persistence of Chlamydia muridarum is determined by macrophage polarization.The subversion of the immune system by francisella tularensis.Alternative activation of macrophages and induction of arginase are not components of pathogenesis mediated by Francisella speciesType II cytokines impair host defense against an intracellular fungal pathogen by amplifying macrophage generation of IL-33.Non-FcεR bearing mast cells secrete sufficient interleukin-4 to control Francisella tularensis replication within macrophagesPreexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway.Increased disease severity of parasite-infected TLR2-/- mice is correlated with decreased central nervous system inflammation and reduced numbers of cells with alternatively activated macrophage phenotypes in a murine model of neurocysticercosis.M1 and M2 macrophages: the chicken and the egg of immunityPotential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza.Deciphering the pathways of death of Histoplasma capsulatum-infected macrophages: implications for the immunopathogenesis of early infection.Targeting of a Fixed Bacterial Immunogen to Fc Receptors Reverses the Anti-Inflammatory Properties of the Gram-Negative Bacterium, Francisella tularensis, during the Early Stages of InfectionDevelopment of tolerogenic dendritic cells and regulatory T cells favors exponential bacterial growth and survival during early respiratory tularemia.An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.Alterations in P-Glycoprotein Expression and Function Between Macrophage Subsets.Respiratory syncytial virus fusion protein-induced toll-like receptor 4 (TLR4) signaling is inhibited by the TLR4 antagonists Rhodobacter sphaeroides lipopolysaccharide and eritoran (E5564) and requires direct interaction with MD-2.Proteomic analysis of bronchoalveolar lavage fluid proteins from mice infected with Francisella tularensis ssp. novicida.
P2860
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P2860
Francisella tularensis live vaccine strain induces macrophage alternative activation as a survival mechanism.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh-hant
name
Francisella tularensis live va ...... ation as a survival mechanism.
@en
Francisella tularensis live va ...... ation as a survival mechanism.
@nl
type
label
Francisella tularensis live va ...... ation as a survival mechanism.
@en
Francisella tularensis live va ...... ation as a survival mechanism.
@nl
prefLabel
Francisella tularensis live va ...... ation as a survival mechanism.
@en
Francisella tularensis live va ...... ation as a survival mechanism.
@nl
P2093
P2860
P1476
Francisella tularensis live va ...... ation as a survival mechanism.
@en
P2093
Achsah D Keegan
Kari Ann Shirey
Leah E Cole
Stefanie N Vogel
P2860
P304
P356
10.4049/JIMMUNOL.181.6.4159
P407
P577
2008-09-01T00:00:00Z