about
MicroRNA as Type I Interferon-Regulated Transcripts and Modulators of the Innate Immune ResponseHero turned villain: NLRP3 inflammasome-induced inflammation during influenza A virus infection.Playing hide and seek: how glycosylation of the influenza virus hemagglutinin can modulate the immune response to infection.Pandemic H1N1 influenza A viruses are resistant to the antiviral activities of innate immune proteins of the collectin and pentraxin superfamilies.PB1-F2 Peptide Derived from Avian Influenza A Virus H7N9 Induces Inflammation via Activation of the NLRP3 Inflammasome.Addition of glycosylation to influenza A virus hemagglutinin modulates antibody-mediated recognition of H1N1 2009 pandemic viruses.Effective pulmonary delivery of an aerosolized plasmid DNA vaccine via surface acoustic wave nebulization.The role of neutrophils during mild and severe influenza virus infections of mice.Critical role of airway macrophages in modulating disease severity during influenza virus infection of mice.N-linked glycosylation facilitates sialic acid-independent attachment and entry of influenza A viruses into cells expressing DC-SIGN or L-SIGNSequence-dependent off-target inhibition of TLR7/8 sensing by synthetic microRNA inhibitorsEndogenous Murine BST-2/Tetherin Is Not a Major Restriction Factor of Influenza A Virus Infection.Soluble host defense lectins in innate immunity to influenza virusThe role of neutrophils in the upper and lower respiratory tract during influenza virus infection of miceGlycosylation as a target for recognition of influenza viruses by the innate immune system.Reassessing the role of the NLRP3 inflammasome during pathogenic influenza A virus infection via temporal inhibitionLoss of a single N-linked glycan from the hemagglutinin of influenza virus is associated with resistance to collectins and increased virulence in mice.The macrophage galactose-type lectin can function as an attachment and entry receptor for influenza virus.Inosine-mediated modulation of RNA sensing by Toll-like receptor 7 (TLR7) and TLR8.Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signalingGlucocorticosteroids enhance replication of respiratory viruses: effect of adjuvant interferon.Cell-surface receptors on macrophages and dendritic cells for attachment and entry of influenza virus.Increased antigen specific T cell numbers in the absence of altered migration or division rates as a result of mucosal cholera toxin administration.Receptor specificity of the influenza virus hemagglutinin modulates sensitivity to soluble collectins of the innate immune system and virulence in mice.Therapeutic Targeting of the IL-6 Trans-Signaling/Mechanistic Target of Rapamycin Complex 1 Axis in Pulmonary Emphysema.Correlation between sialic acid expression and infection of murine macrophages by different strains of influenza virus.Inhibition of lectin-mediated innate host defences in vivo modulates disease severity during influenza virus infection.Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice.Highly pathogenic avian H5N8 influenza viruses: Should we be concerned?SIDT2 Transports Extracellular dsRNA into the Cytoplasm for Innate Immune Recognition.Gr-1+ cells, but not neutrophils, limit virus replication and lesion development following flank infection of mice with herpes simplex virus type-1.Specific sites of N-linked glycosylation on the hemagglutinin of H1N1 subtype influenza A virus determine sensitivity to inhibitors of the innate immune system and virulence in mice.Responses of mouse airway epithelial cells and alveolar macrophages to virulent and avirulent strains of influenza A virus.Depletion of Gr-1+, but not Ly6G+, immune cells exacerbates virus replication and disease in an intranasal model of herpes simplex virus type 1 infection.Defining the distinct, intrinsic properties of the novel type I interferon, epsilon.Antiviral activity of the long chain pentraxin PTX3 against influenza viruses.In Vivo Infection Model of Severe Influenza A Virus.Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation.Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza InfectionTANKing Influenza A Virus in the Lung
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description
hulumtuese
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researcher
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հետազոտող
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name
Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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Michelle D. Tate
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22939334200
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P31
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0000-0002-0587-5514