Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis - Test2 - elhamkhani - TriplyDB

Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis

Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis

http://www.wikidata.org/entity/Q28485277

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From the Outside-In: The Francisella tularensis Envelope and Virulence Macrophage proliferation, provenance, and plasticity in macroparasite infection Comparative review of Francisella tularensis and Francisella novicida Adherence and uptake of Francisella into host cells Lyn regulates inflammatory responses in Klebsiella pneumoniae infection via the p38/NF-κB pathway.The impact of "omic" and imaging technologies on assessing the host immune response to biodefence agents.Differential expression of microRNAs in Francisella tularensis-infected human macrophages: miR-155-dependent downregulation of MyD88 inhibits the inflammatory response.Virulent Francisella tularensis destabilize host mRNA to rapidly suppress inflammation.Complement opsonization of HIV-1 results in decreased antiviral and inflammatory responses in immature dendritic cells via CR3 Needle-Free Delivery of Acetalated Dextran-Encapsulated AR-12 Protects Mice from Francisella tularensis Lethal Challenge.Playing hide-and-seek with host macrophages through the use of mycobacterial cell envelope phthiocerol dimycocerosates and phenolic glycolipids Phagocytosis via complement or Fc-gamma receptors is compromised in monocytes from type 2 diabetes patients with chronic hyperglycemia.Inflammasome priming is similar for francisella species that differentially induce inflammasome activation.PE_PGRS33 Contributes to Mycobacterium tuberculosis Entry in Macrophages through Interaction with TLR2 Identification of Genes Required for Secretion of the Francisella Oxidative Burst-Inhibiting Acid Phosphatase AcpA.Early Interactions of Murine Macrophages with Francisella tularensis Map to Mouse Chromosome 19 Complement Opsonization Promotes Herpes Simplex Virus 2 Infection of Human Dendritic Cells.Francisella tularensis - Immune Cell Activator, Suppressor, or Stealthy Evader: The Evolving View from the Petri Dish.Lyn mitigates mouse airway remodeling by downregulating the TGF-β3 isoform in house dust mite models.Hijacking Complement Regulatory Proteins for Bacterial Immune Evasion.Leishmania major inhibits IL-12 in macrophages by signalling through CR3 (CD11b/CD18) and down-regulation of ETS-mediated transcription.Serving the new masters - dendritic cells as hosts for stealth intracellular bacteria.Monocyte/macrophage inflammatory response pathways to combat Francisella infection: possible therapeutic targets?Complement, c1q, and c1q-related molecules regulate macrophage polarization.Biomolecular engineering of virus-like particles aided by computational chemistry methods.Let's Tie the Knot: Marriage of Complement and Adaptive Immunity in Pathogen Evasion, for Better or Worse.Francisella novicida inhibits spontaneous apoptosis and extends human neutrophil lifespan.Induction of Central Host Signaling Kinases during Pneumococcal Infection of Human THP-1 Cells Virulent Type A Francisella tularensis actively suppresses cytokine responses in human monocytes Mathematical Models for Immunology: Current State of the Art and Future Research Directions.Francisella Inflammasomes: Integrated Responses to a Cytosolic Stealth Bacterium.Multifaceted effects of Francisella tularensis on human neutrophil function and lifespan.More than complementing Tolls: complement-Toll-like receptor synergy and crosstalk in innate immunity and inflammation.Complement C3 as a Prompt for Human Macrophage Death during Infection with Francisella tularensis Strain SCHU S4.Modeling early events in Francisella tularensis pathogenesis.Correction: Fine Tuning Inflammation at the Front Door: Macrophage Complement Receptor 3-mediates Phagocytosis and Immune Suppression for Francisella tularensis.Innate Immune Recognition: Implications for the Interaction of Francisella tularensis with the Host Immune System.Novel mechanisms and functions of complement.Bacterial lipoproteins and other factors released by Francisella tularensis modulate human neutrophil lifespan: Effects of a TLR1 SNP on apoptosis inhibition.Francisella tularensis Confronts the Complement System.

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Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis

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Fine tuning inflammation at th ...... ion for Francisella tularensis

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Heather M Curry

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Larry S Schlesinger

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Murugesan V S Rajaram

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Rachel Leander

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Shipan Dai

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MiR-155 induction by F. novicida but not the virulent F. tularensis results in SHIP down-regulation and enhanced pro-inflammatory cytokine response

NOD2 controls the nature of the inflammatory response and subsequent fate of Mycobacterium tuberculosis and M. bovis BCG in human macrophages

A TIR domain variant of MyD88 adapter-like (Mal)/TIRAP results in loss of MyD88 binding and reduced TLR2/TLR4 signaling

C1q and mannose binding lectin engagement of cell surface calreticulin and CD91 initiates macropinocytosis and uptake of apoptotic cells

Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3

Microarray analysis of human monocytes infected with Francisella tularensis identifies new targets of host response subversion

Integrin CD11b negatively regulates TLR-triggered inflammatory responses by activating Syk and promoting degradation of MyD88 and TRIF via Cbl-b

Activation of murine macrophages via TLR2 and TLR4 is negatively regulated by a Lyn/PI3K module and promoted by SHIP1

TLR-dependent control of Francisella tularensis infection and host inflammatory responses

Complement: a key system for immune surveillance and homeostasis

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