Group A streptococcus activates type I interferon production and MyD88-dependent signaling without involvement of TLR2, TLR4, and TLR9. - Wikidata - wikimedia - TriplyDB

Group A streptococcus activates type I interferon production and MyD88-dependent signaling without involvement of TLR2, TLR4, and TLR9.

Group A streptococcus activates type I interferon production and MyD88-dependent signaling without involvement of TLR2, TLR4, and TLR9.

http://www.wikidata.org/entity/Q40088398

about

Immune evasion and recognition of the syphilis spirochete in blood and skin of secondary syphilis patients: two immunologically distinct compartments Inflammasome/IL-1β Responses to Streptococcal Pathogens Phagosomal signaling by Borrelia burgdorferi in human monocytes involves Toll-like receptor (TLR) 2 and TLR8 cooperativity and TLR8-mediated induction of IFN-beta The innate immune response elicited by Group A Streptococcus is highly variable among clinical isolates and correlates with the emm type.Activation of human monocytes by live Borrelia burgdorferi generates TLR2-dependent and -independent responses which include induction of IFN-beta.Borrelia burgdorferi RNA induces type I and III interferons via Toll-like receptor 7 and contributes to production of NF-κB-dependent cytokines Bifidobacterium bifidum actively changes the gene expression profile induced by Lactobacillus acidophilus in murine dendritic cells.Type I interferon production induced by Streptococcus pyogenes-derived nucleic acids is required for host protection MyD88 and STING signaling pathways are required for IRF3-mediated IFN-β induction in response to Brucella abortus infection Responses of innate immune cells to group A Streptococcus.Macrophages recognize streptococci through bacterial single-stranded RNA A critical role for type I IFN in arthritis development following Borrelia burgdorferi infection of mice.Streptococcus pneumoniae DNA initiates type I interferon signaling in the respiratory tract Innate immune response to Streptococcus pyogenes depends on the combined activation of TLR13 and TLR2.Host responses to group a streptococcus: cell death and inflammation Postpartum group a Streptococcus sepsis and maternal immunology.NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA Importance of Toll-like receptor 9 in host defense against M1T1 group A Streptococcus infections A MyD88-JAK1-STAT1 complex directly induces SOCS-1 expression in macrophages infected with Group A Streptococcus.Failure to induce IFN-β production during Staphylococcus aureus infection contributes to pathogenicity.Regulatory role of GSK-3 β on NF- κ B, nitric oxide, and TNF- α in group A streptococcal infection.Exacerbated type II interferon response drives hypervirulence and toxic shock by an emergent epidemic strain of Streptococcus suis CDK8-mediated STAT1-S727 phosphorylation restrains NK cell cytotoxicity and tumor surveillance Activation of the Nlrp3 inflammasome by Streptococcus pyogenes requires streptolysin O and NF-kappa B activation but proceeds independently of TLR signaling and P2X7 receptor.The Emerging Roles of STING in Bacterial Infections.The role of innate immune signals in immunity to Brucella abortus.Subterfuge and sabotage: evasion of host innate defenses by invasive gram-positive bacterial pathogens.Lactobacillus acidophilus induces virus immune defence genes in murine dendritic cells by a Toll-like receptor-2-dependent mechanism.Superoxide anions produced by Streptococcus pyogenes group A-stimulated keratinocytes are responsible for cellular necrosis and bacterial growth inhibition.Group A Streptococcus emm3 strains induce early macrophage cell death.The Lyme disease spirochete Borrelia burgdorferi utilizes multiple ligands, including RNA, for interferon regulatory factor 3-dependent induction of type I interferon-responsive genes A critical role for hemolysins and bacterial lipoproteins in Staphylococcus aureus-induced activation of the Nlrp3 inflammasome.Invasive group A Streptococcus disease in French-Canadian children is not associated with a defect in MyD88/IRAK4-pathway Dynamin inhibition interferes with inflammasome activation and cytokine gene expression in Streptococcus pyogenes-infected human macrophages.Aberrant inflammatory response to Streptococcus pyogenes in mice lacking myeloid differentiation factor 88.Group A Streptococcus encounters with host macrophages.Streptococcal M protein promotes IL-10 production by cGAS-independent activation of the STING signaling pathway.Mechanisms of TNF induction by heat-killed Staphylococcus aureus differ upon the origin of mononuclear phagocytes.Dextromethorphan Attenuates NADPH Oxidase-Regulated Glycogen Synthase Kinase 3β and NF-κB Activation and Reduces Nitric Oxide Production in Group A Streptococcal Infection.The Bicarbonate Transporter SLC4A7 Plays a Key Role in Macrophage Phagosome Acidification.

P2860

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P2860

Group A streptococcus activates type I interferon production and MyD88-dependent signaling without involvement of TLR2, TLR4, and TLR9.

http://www.wikidata.org/entity/Q40088398

description

2008 nî lūn-bûn

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Group A streptococcus activate ...... ement of TLR2, TLR4, and TLR9.

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Group A streptococcus activate ...... ement of TLR2, TLR4, and TLR9.

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Group A streptococcus activate ...... ement of TLR2, TLR4, and TLR9.

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Group A streptococcus activate ...... ement of TLR2, TLR4, and TLR9.

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Barbara Schaljo

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Carsten J Kirschning

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Hermann Wagner

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Irene Gattermeier

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Ivo Vojtek

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Maria Siller

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Nina Gratz

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Shizuo Akira

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Zaid A Pirzada

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P2860

Molecular genetic anatomy of inter- and intraserotype variation in the human bacterial pathogen group A Streptococcus

A Toll-like receptor recognizes bacterial DNA

DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response

Cytotoxic effects of streptolysin o and streptolysin s enhance the virulence of poorly encapsulated group a streptococci

NOD2 and toll-like receptors are nonredundant recognition systems of Mycobacterium tuberculosis

Viable group A streptococci in macrophages during acute soft tissue infection

An Atomic Model of the Interferon-β Enhanceosome

Pathogen recognition and innate immunity

Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product

IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway

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19879-19887

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10.1074/JBC.M802848200

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29

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283

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Emmanuelle Charpentier

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18480050

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2459277

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