Disease relevance of Arthritis, Rheumatoid

• Therapies that neutralize the function of TNF-alpha suppress rheumatoid arthritis (RA) but not osteoarthritis (OA) [1].
• Chronic inflammatory autoimmune diseases such as multiple sclerosis, diabetes, and rheumatoid arthritis are caused by CD4(+) Th1 cells [2].
• Our results reveal a critical role for G-CSF in driving joint inflammation and highlight G-CSF as a potential therapeutic target in inflammatory joint diseases, such as rheumatoid arthritis [3].
• CONCLUSION: These results indicate that IFNbeta, which is currently used as a treatment for relapsing, remitting multiple sclerosis, is a potent immunomodulatory and antiinflammatory cytokine in CIA and should be considered for the treatment of rheumatoid arthritis [4].
• Japanese patients with primary Sjögren's syndrome (SS), patients with SS and rheumatoid arthritis (SS-RA), and patients with SS and connective tissue disease without RA (nonrheumatoid connective tissue disease [SS-CTD]) were typed for HLA antigens [5].

High impact information on Arthritis, Rheumatoid

• We also describe that oral treatment with a PI3Kgamma inhibitor suppresses the progression of joint inflammation and damage in two distinct mouse models of rheumatoid arthritis, reproducing the protective effects shown by Pik3cg(-/-) mice [6].
• IFN-gamma signaling was sensitized in vivo after IFN-gamma injection, and STAT1 expression was increased after injection of lipopolysaccharide and in rheumatoid arthritis synovial cells [7].
• In the K/BxN mouse model of rheumatoid arthritis, the transfer of autoantibodies specific for glucose-6-phosphate isomerase (GPI) into naïve mice rapidly induces joint-specific inflammation similar to that seen in human rheumatoid arthritis [8].
• Prostaglandin (PG)I2 (prostacyclin [PGI]) and PGE2 are abundantly present in the synovial fluid of rheumatoid arthritis (RA) patients [9].
• IL-10 signaling was suppressed in rheumatoid arthritis joint macrophages that are exposed to immune complexes in vivo [10].

Chemical compound and disease context of Arthritis, Rheumatoid

• Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin alphavbeta3 [11].
• Letter: Clotrimazole and rheumatoid arthritis [12].
• A large body of correlative data (including remission of arthritis during pregnancy) has suggested that IgG molecules lacking galactose were associated with rheumatoid arthritis [13].
• IL-7, a powerful lymphopoietic cytokine, is elevated in rheumatoid arthritis (RA) and known to induce bone loss when administered in vivo [14].
• OBJECTIVE: Weekly low-dose methotrexate (MTX) remains the mainstay of second-line therapy for rheumatoid arthritis (RA) [15].
• Guidelines for introducing TNFalpha antagonists in rheumatoid arthritis often fail to meet expected methodologic criteria and therefore vary significantly in quality and with respect to some recommendations for patient assessment and management [16].

Biological context of Arthritis, Rheumatoid

• These results indicated that OPN plays a critical role in the destruction of joint cartilage in the rheumatoid arthritis model in mice via promotion of angiogenesis and induction of chondrocyte apoptosis [17].
• OBJECTIVE: To determine if tumor necrosis factor alpha (TNFalpha)-driven proliferation of rheumatoid arthritis synovial fibroblasts (RASF) is associated with up-regulation of the activity of serine/threonine kinase B/Akt and with survival of RASF [18].
• Proteoglycan-induced arthritis (PGIA) is a murine model for rheumatoid arthritis (RA) both in terms of its pathology and its genetics [19].
• The Toll-like receptor 4 Asp299Gly functional variant is associated with decreased rheumatoid arthritis disease susceptibility but does not influence disease severity and/or outcome [20].
• OBJECTIVE: To assess the intra- and interreader reliability and the sensitivity to change of the Outcome Measures in Rheumatology Clinical Trials (OMERACT) Rheumatoid Arthritis Magnetic Resonance Imaging Score (RAMRIS) system on digital images of the wrist joints of patients with early or established rheumatoid arthritis (RA) [21].

Anatomical context of Arthritis, Rheumatoid

• Interleukin-6 (IL-6) is overproduced in the joints of patients with rheumatoid arthritis (RA) and, based on its multiple stimulatory effects on cells of the immune system and on vascular endothelia, osteoclasts, and synovial fibroblasts, is believed to participate in the development and clinical manifestations of this disease [22].
• Activated lymphocytes and synoviocytes from patients with rheumatoid arthritis express receptors that can bind TNF-related apoptosis-inducing ligand (TRAIL) [23].
• In both rheumatoid arthritis and animal models of autoimmune arthritis, high levels of Fas are expressed on activated synovial cells and infiltrating leukocytes in the inflamed joints [24].
• The potential of IL-4 to promote inflammatory arthritis should be considered when proposing therapies for rheumatoid arthritis aimed at biasing T cells toward IL-4 production [25].
• We have determined the relationship of antibody titers to the rheumatoid arthritis nuclear antigen (RANA) and of antibody titers to the Epstein-Barr nuclear antigen (EBNA) to each other and to the DRw4 B cell alloantigen in the sera of 34 normal white adults [26].

Gene context of Arthritis, Rheumatoid

• Mitogen-activated protein kinase (MAPK) cascades are involved in inflammation and tissue destruction in rheumatoid arthritis (RA) [27].
• Disregulation of TNF-alpha is associated with sepsis and autoimmune diseases such as rheumatoid arthritis [28].
• To clarify these roles, we investigated the development of Ab-induced arthritis, one of the murine models of rheumatoid arthritis, in MMP-2 or MMP-9 knockout (KO) mice [29].
• Together, these results argue that Ncf1 is not a candidate gene for regulation of Lyme arthritis and reveal Lyme arthritis to be independent of NADPH oxidase activity, distinguishing it from other models of rheumatoid arthritis [30].
• INTRODUCTION: Rheumatoid arthritis (RA) is associated with focal and systemic bone loss involving cytokines such as RANKL and TNF-alpha [31].

Analytical, diagnostic and therapeutic context of Arthritis, Rheumatoid

• Inhibition of interleukin 10 signaling after Fc receptor ligation and during rheumatoid arthritis [10].
• We have engineered bone marrow-derived DCs that express IL-4 and tested the ability of these cells to control murine collagen-induced arthritis (CIA), a model for rheumatoid arthritis in which Th1 cells play a critical role [32].
• These results suggest that vaccination against TNF-alpha may be a useful approach for the treatment of rheumatoid arthritis and other chronic inflammatory diseases [33].
• OBJECTIVE: Clinical trials using interferon-beta (IFNbeta) in the treatment of rheumatoid arthritis have shown conflicting results [34].
• A cell-free extract of human diploid B lymphocytes (Wil2) in continuous culture was used as the source of antigen in immunodiffusion to detect a precipitating antibody referred to as rheumatoid arthritis precipitin (RAP) in sera of patients with rheumatoid arthritis (RA) [35].

References