IL-17A deficiency promotes periosteal bone formation in a model of inflammatory arthritis. - Wikidata - awgldk - TriplyDB

IL-17A deficiency promotes periosteal bone formation in a model of inflammatory arthritis.

IL-17A deficiency promotes periosteal bone formation in a model of inflammatory arthritis.

http://www.wikidata.org/entity/Q41353840

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Mechanism of New Bone Formation in Axial Spondyloarthritis.Differential Effects of Inflammation on Bone and Response to Biologics in Rheumatoid Arthritis and Spondyloarthritis.Autoimmunity as a trigger for structural bone damage in rheumatoid arthritis.Cellular and molecular pathways of structural damage in rheumatoid arthritis.Bone loss and aggravated autoimmune arthritis in HLA-DRβ1-bearing humanized mice following oral challenge with Porphyromonas gingivalis Bone Wasn't Built in a Day: Destruction and Formation of Bone in the Rheumatic Diseases.Targeting IL-17 in psoriatic arthritis.Altered Bone Remodeling in Psoriatic Disease: New Insights and Future Directions.Bone Loss in Rheumatoid Arthritis: Basic Mechanisms and Clinical Implications.Tumor Necrosis Factor Alpha Overexpression Induces Mainly Osteoclastogenesis at the Vertebral Site.The role of IL-23 receptor signaling in inflammation-mediated erosive autoimmune arthritis and bone remodeling.What is the best treatment target in axial spondyloarthritis: tumour necrosis factor α, interleukin 17, or both?Interleukin 17 enhances bone morphogenetic protein-2-induced ectopic bone formation.

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IL-17A deficiency promotes periosteal bone formation in a model of inflammatory arthritis.

http://www.wikidata.org/entity/Q41353840

description

2016 nî lūn-bûn

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2016年の論文

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2016年論文

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2016年論文

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2016年论文

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2016年论文

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Anita T Shaw

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Ellen M Gravallese

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Yukiko Maeda

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P2860

IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis

T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Expression of the calcitonin receptor in bone marrow cell cultures and in bone: a specific marker of the differentiated osteoclast that is regulated by calcitonin

Worsening of pain and function over 5 years in individuals with 'early' OA is related to structural damage: data from the Osteoarthritis Initiative and CHECK (Cohort Hip & Cohort Knee) study.

IL-17-producing T cells can augment autoantibody-induced arthritis

A bone-protective role for IL-17 receptor signaling in ovariectomy-induced bone loss.

From systemic T cell self-reactivity to organ-specific autoimmune disease via immunoglobulins.

IL-17RA signaling amplifies antibody-induced arthritis.

TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis.

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