Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
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Host response mechanisms in periodontal diseasesInactive Gingipains from P. gingivalis Selectively Skews T Cells toward a Th17 Phenotype in an IL-6 Dependent MannerTLR2 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 pathogenIL-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 pericoronitisRadiolucency below the crown of mandibular horizontal incompletely impacted third molars and acute inflammation in men with diabetes.Therapeutic Targets for Management of Periodontitis and DiabetesInterrelationship 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-5Mucosal Langerhans Cells Promote Differentiation of Th17 Cells in a Murine Model of Periodontitis but Are Not Required for Porphyromonas gingivalis-Driven Alveolar Bone DestructionA 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 infectionsHow 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.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@ast
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@en
type
label
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@ast
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@en
prefLabel
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@ast
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@en
P2093
P2860
P1476
Th1 immune response promotes severe bone resorption caused by Porphyromonas gingivalis.
@en
P2093
Alexander Ficarelli
Antonio Campos-Neto
Brad Lipkin
Hajime Sasaki
Philip Stashenko
Reginaldo B Gonçalves
P2860
P304
P356
10.2353/AJPATH.2007.060597
P407
P577
2007-01-01T00:00:00Z