Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis. - Wikidata - awgldk - TriplyDB

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

http://www.wikidata.org/entity/Q35570427

about

Host response mechanisms in periodontal diseases Inactive Gingipains from P. gingivalis Selectively Skews T Cells toward a Th17 Phenotype in an IL-6 Dependent Manner TLR2 signaling and Th2 responses drive Tannerella forsythia-induced periodontal bone loss.CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model.Effects of periodontal therapy on GCF cytokines in generalized aggressive periodontitis subjects.Th1 biased response to a novel Porphyromonas gingivalis protein aggravates bone resorption caused by this oral pathogen IL-4 and IL-13 inhibit IL-1β and TNF-α induced kinin B1 and B2 receptors through a STAT6-dependent mechanism.Bone resorption in incompletely impacted mandibular third molars and acute pericoronitis Radiolucency below the crown of mandibular horizontal incompletely impacted third molars and acute inflammation in men with diabetes.Therapeutic Targets for Management of Periodontitis and Diabetes Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders.p38 MAPK signaling in oral-related diseases.Immune response and alveolar bone resorption in a mouse model of Treponema denticola infection.The RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis Inactivate the Th2 cytokines interleukin-4 and interleukin-5 Mucosal Langerhans Cells Promote Differentiation of Th17 Cells in a Murine Model of Periodontitis but Are Not Required for Porphyromonas gingivalis-Driven Alveolar Bone Destruction A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17.Kinin danger signals proteolytically released by gingipain induce Fimbriae-specific IFN-gamma- and IL-17-producing T cells in mice infected intramucosally with Porphyromonas gingivalis.Interleukin-1 and estrogen protect against disseminating dentoalveolar infections How has research into cytokine interactions and their role in driving immune responses impacted our understanding of periodontitis?Role of osteoclasts and interleukin-17 in the pathogenesis of rheumatoid arthritis: crucial 'human osteoclastology'.Dendritic cells and their role in periodontal disease.Macrophage subsets and osteoimmunology: tuning of the immunological recognition and effector systems that maintain alveolar bone.The innate host response in caries and periodontitis.Protective role of osteopontin in endodontic infection.Therapeutic Targets for Management of Periodontitis and Diabetes.A therapeutic Porphyromonas gingivalis gingipain vaccine induces neutralising IgG1 antibodies that protect against experimental periodontitis.Porphyromonas gingivalis induces RANKL in T-cells.

P2860

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P2860

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

http://www.wikidata.org/entity/Q35570427

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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prefLabel

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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The American Journal of Pathology

P1476

Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.

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P2093

Alexander Ficarelli

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Antonio Campos-Neto

http://www.w3.org/2001/XMLSchema#string

Brad Lipkin

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Hajime Sasaki

http://www.w3.org/2001/XMLSchema#string

Philip Stashenko

http://www.w3.org/2001/XMLSchema#string

Reginaldo B Gonçalves

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P2860

IFN-gamma-producing human T cells directly induce osteoclastogenesis from human monocytes via the expression of RANKL

Interleukin-6 deficiency increases inflammatory bone destruction

T-cell expression cloning of Porphyromonas gingivalis genes coding for T helper-biased immune responses during infection

Cytokine patterns in the pathogenesis of human leishmaniasis.

Protection against cutaneous leishmaniasis induced by recombinant antigens in murine and nonhuman primate models of the human disease.

Involvement of T-lymphocytes in periodontal disease and in direct and indirect induction of bone resorption.

Regulatory mechanisms of osteoblast and osteoclast differentiation.

Interleukin-10 inhibits gram-negative-microbe-specific human receptor activator of NF-kappaB ligand-positive CD4+-Th1-cell-associated alveolar bone loss in vivo

Immunopathogenesis of collagen arthritis.

Inter-relationships between rheumatoid arthritis and periodontal disease. A review.

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170

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6601074

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17200194

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Porphyromonas gingivalis

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1762702

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