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How has neutrophil research improved our understanding of periodontal pathogenesis?

Journal of clinical periodontology, 2011-03, Vol.38 (s11), p.49-59

2011

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Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion

PLoS pathogens, 2023-04, Vol.19 (4), p.e1011284-e1011284

2023

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Periodontal pathogens Porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model

Oncotarget, 2015-09, Vol.6 (26), p.22613-22623

2015

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Porphyromonas gingivalis Manipulates Complement and TLR Signaling to Uncouple Bacterial Clearance from Inflammation and Promote Dysbiosis

Cell host & microbe, 2014-06, Vol.15 (6), p.768-778

2014

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Cutting Edge: TLR2 Is Required for the Innate Response to Porphyromonas gingivalis: Activation Leads to Bacterial Persistence and TLR2 Deficiency Attenuates Induced Alveolar Bone Resorption

The Journal of immunology (1950), 2006-12, Vol.177 (12), p.8296-8300

2006

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GAS6 is a key homeostatic immunological regulator of host–commensal interactions in the oral mucosa

Proceedings of the National Academy of Sciences - PNAS, 2017-01, Vol.114 (3), p.E337-E346

2017

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Porphyromonas gingivalis Stimulates TLR2-PI3K Signaling to Escape Immune Clearance and Induce Bone Resorption Independently of MyD88

Frontiers in cellular and infection microbiology, 2017-08, Vol.7, p.359-359

2017

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Oral fibroblasts modulate the macrophage response to bacterial challenge

Scientific reports, 2017-09, Vol.7 (1), p.11516-11, Article 11516

2017

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Intracellular Porphyromonas gingivalis Promotes the Tumorigenic Behavior of Pancreatic Carcinoma Cells

Cancers, 2020-08, Vol.12 (8), p.2331

2020

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TLR2-Dependent Inflammatory Response to Porphyromonas gingivalis Is MyD88 Independent, whereas MyD88 Is Required To Clear Infection

The Journal of immunology (1950), 2010-02, Vol.184 (3), p.1455-1462

2010

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The cationic liposome CCS/C adjuvant induces immunity to influenza independently of the adaptor protein MyD88

Human vaccines & immunotherapeutics, 2020-12, Vol.16 (12), p.3146-3154

2020

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Syndecan-1 deficiency promotes tumor growth in a murine model of colitis-induced colon carcinoma

PloS one, 2017-03, Vol.12 (3), p.e0174343-e0174343

2017

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Porphyromonas gingivalis Gingipains Selectively Reduce CD14 Expression, Leading to Macrophage Hyporesponsiveness to Bacterial Infection

Journal of innate immunity, 2015-01, Vol.7 (2), p.127-135

2015

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Porphyromonas gingivalis Promotes Unrestrained Type I Interferon Production by Dysregulating TAM Signaling via MYD88 Degradation

Cell reports (Cambridge), 2017-01, Vol.18 (2), p.419-431

2017

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Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway

PLoS pathogens, 2017-07, Vol.13 (7), p.e1006472-e1006472

2017

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Heat Shock Protein 60 Activates B Cells via the TLR4-MyD88 Pathway

The Journal of immunology (1950), 2005-09, Vol.175 (6), p.3594-3602

2005

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Involvement of Toll-Like Receptors 2 and 4 in the Innate Immune Response to Treponema denticola and Its Outer Sheath Components

Infection and Immunity, 2009-09, Vol.77 (9), p.3939-3947

2009

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The contrastive poetics of short genres in Russian and Tatar literature

Revista EntreLínguas (Online), 2021, Vol.7 (8)

2021

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Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice

Frontiers in immunology, 2017-05, Vol.8, p.615-615

2017

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From bedside to the bench: uncovering the role of a T-cell protein in protecting CTLA-4

Oral diseases, 2016-05, Vol.22 (4), p.249-250

Nussbaum, Gabriel

2016

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Peptide p277 of HSP60 signals T cells: inhibition of inflammatory chemotaxis

International immunology, 2006-10, Vol.18 (10), p.1413-1419

2006

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Induction of IgG3 to LPS via Toll-like receptor 4 co-stimulation

PloS one, 2008-10, Vol.3 (10), p.e3509-e3509

2008

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Oral infection with Porphyromonas gingivalis induces peri‐implantitis in a murine model: Evaluation of bone loss and the local inflammatory response

Journal of clinical periodontology, 2017-07, Vol.44 (7), p.739-748

2017

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Macrophage Polarization in Pancreatic Carcinoma: Role of Heparanase Enzyme

JNCI : Journal of the National Cancer Institute, 2014-12, Vol.106 (12), p.1

2014

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Macrophage activation by heparanase is mediated by TLR-2 and TLR-4 and associates with plaque progression

Arteriosclerosis, thrombosis, and vascular biology, 2013-02, Vol.33 (2), p.e56

2013

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How has neutrophil research improved our understanding of periodontal pathogenesis?

Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion

Periodontal pathogens Porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model

Porphyromonas gingivalis Manipulates Complement and TLR Signaling to Uncouple Bacterial Clearance from Inflammation and Promote Dysbiosis

Cutting Edge: TLR2 Is Required for the Innate Response to Porphyromonas gingivalis: Activation Leads to Bacterial Persistence and TLR2 Deficiency Attenuates Induced Alveolar Bone Resorption

GAS6 is a key homeostatic immunological regulator of host–commensal interactions in the oral mucosa

Porphyromonas gingivalis Stimulates TLR2-PI3K Signaling to Escape Immune Clearance and Induce Bone Resorption Independently of MyD88

Oral fibroblasts modulate the macrophage response to bacterial challenge

Intracellular Porphyromonas gingivalis Promotes the Tumorigenic Behavior of Pancreatic Carcinoma Cells

TLR2-Dependent Inflammatory Response to Porphyromonas gingivalis Is MyD88 Independent, whereas MyD88 Is Required To Clear Infection

The cationic liposome CCS/C adjuvant induces immunity to influenza independently of the adaptor protein MyD88

Syndecan-1 deficiency promotes tumor growth in a murine model of colitis-induced colon carcinoma

Porphyromonas gingivalis Gingipains Selectively Reduce CD14 Expression, Leading to Macrophage Hyporesponsiveness to Bacterial Infection

Porphyromonas gingivalis Promotes Unrestrained Type I Interferon Production by Dysregulating TAM Signaling via MYD88 Degradation

Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway

Heat Shock Protein 60 Activates B Cells via the TLR4-MyD88 Pathway

Involvement of Toll-Like Receptors 2 and 4 in the Innate Immune Response to Treponema denticola and Its Outer Sheath Components

The contrastive poetics of short genres in Russian and Tatar literature

Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice

From bedside to the bench: uncovering the role of a T-cell protein in protecting CTLA-4

Peptide p277 of HSP60 signals T cells: inhibition of inflammatory chemotaxis

Induction of IgG3 to LPS via Toll-like receptor 4 co-stimulation

Oral infection with Porphyromonas gingivalis induces peri‐implantitis in a murine model: Evaluation of bone loss and the local inflammatory response

Macrophage Polarization in Pancreatic Carcinoma: Role of Heparanase Enzyme

Macrophage activation by heparanase is mediated by TLR-2 and TLR-4 and associates with plaque progression

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