View clinical trials related to Rheumatoid Arthritis.
Filter by:The purpose of this study is to evaluate the value of Quantiferon-TB Gold (QFT-G) assay in the screening for latent tuberculosis infection (LTBI) in rheumatologic patients due to start or on treatment with TNFα antagonists. The results of QFT-G will be compared to tuberculin skin testing (TST) and correlated to clinical and demographic data. The study hypothesis is that the inclusion of QTF-G in the screening strategy will allow a more accurate assessment of LTBI infection.
Over the past few years, growing evidences revealed that clearance of apoptotic cells by phagocytosis can result in powerful anti-inflammatory and immunosuppressive effects. In vivo, apoptotic cells are cleared rapidly by neighboring cells, macrophages and related scavengers. Defective clearance of apoptotic cells has been linked closely to autoimmunity and persistent inflammatory disease. Several phagocytic receptors, bridging molecules produced by phagocytes and 'eat-me' signals on apoptotic cells are coordinately involved in mediating clearance of apoptotic cells. Complement receptors (CR3, CR4), collection, CD14, CD36 (Class B scavenger receptor), class A scavenger receptor, asialoprotein receptor, Mer receptor kinase were reported to recognize apoptotic cells. The best characterized system for clearance of apoptotic cells is the recognition of phosphatidylserine (PS) on apoptotic cells by phosphatidylserine receptor (PSR). Milk fat globule- epidermal growth factor 8 (MFG-E8) is an opsonin that bridges phagocytes (by interacting with α vβ3, αvβ5 integrins via RGD motif) and apoptotic cells (by binding PS through Factor V/VIII-C domain). Activated macrophages produce and secret MFG-E8. MFG-E8 is a critical component in PSR-mediated phagocytosis of apoptotic cells. The dominant negative mutant MFG-E8, D89E, that carried a mutated RGD motif inhibited phagocytosis of apoptotic cells in vitro. Injection of D89E into wild type mice induced autoantibodies and IgG deposition on glomeruli. Macrophages from MFG-E8 deficiency (MFG-E8-/-) mice were impaired in engulfment of apoptotic cells, which can be restored by adding recombinant MFG-E8. The female MFG-E8-/- mice spontaneously produced high titer of autoantibodies and developed lupus-like glomerulonephritis at the age of week 40. Defective clearance of apoptotic cells is closely related to development of autoimmunity. In the past 4 years, a growing number of molecules were recognized as receptors for the PS exposed on the apoptotic cells. These molecules were capable of mediating phagocytic clearance, rendering anti-inflammatory cytokines in the phagocytes, and modulating T cell responses. The specific aim of this proposal is to study genetic polymorphism in MFG-E8, PSR and other factors implicated in phagocytic clearance of apoptotic cells among Taiwanese. By comparing the polymorphism between patients with autoimmune disease (SLE or RA) and healthy control subjects, we will investigate if genetic variations among individuals of genes encoding proteins involved in clearance of apoptotic cells contribute to the pathogenesis of systemic autoimmune diseases SLE and RA.
The main aim of this study is to identify genetic markers (at DNA and RNA level) which are involved in the response to treatment with monoclonal antibodies against TNF in patients with rheumatoid arthritis.
Evaluation of two treatment modalities in early potentially severe early arthritis ( Methotrexate alone or in combination with adalimumab)
As one of the characteristic clinical features of the patients with rheumatoid arthritis, the unique character of the patients, somewhat difficult to be persuaded but theoretical, has long been pointed out. The investigators hypothesized that this unique character might be due to the sleep disturbance in the patients possibly due to severe pain of arthritis or unique biochemical disease activities. The investigators test (1) the sleep quality of the patients and draw some characteristic features, and (2) investigated the connection between unique biochemical changes such as the increase of c-fos or wee-1.
The purpose of this study is to identify differences in TB specific immune responses among immunosuppressed patients latently infected with TB and patients with active TB.
Decoy receptor 3 (DcR3), a new member of tumor necrosis factor receptor (TNFR) superfamily, is a decoy receptor for FasL and could inhibit FasL-induced apoptosis, has recently been shown to induce costimulation of T cells. Systemic lupus erythematosus (SLE) is an autoimmune disease with pathogenic autoantibodies and immune complexes results from abnormal immune responses including T and B lymphocyte hyperactivity, and formation of pathogenic subsets of autoantibodies. Rhematoid arthritis (RA) is a multi-systemic autoimmune disease characterized by persistent inflammatory synovitis. Activated T lymphocytes infiltration to synovium is strongly correlated with the symptoms. DcR3 mRNA is expressed in peripheral-blood T cells and is up-regulated after antigenic stimulation. The DcR3 gene has been demonstrated to be overexpressed in patients with sclerosis or SLE; however, role of DcR3 in SLE and RA as well as the effects of DcR3 on T cell immune response is still not clear. This study is to investigate role of DcR3-induced T cell activation in SLE and RA. The genetic polymorphisms of DcR3 in association with SLE and RA will be studied to elucidate the genetic factors associated with development of SLE and RA. For further explore the possible molecular mechanisms of elevated DcR3 in association with SLE, we attempt to study whether DcR3 could induce T cell activation via costimualtion and/or inhibit the activation induced cell death (AICD) of activated T cells in SLE and RA. This study will provide a new direction of therapy in reverse T cell hyper-reactivity in SLE and RA.
The purpose of this study is to establish whether RA patients with moderate to severe disease activity with unsustainable response to infliximab 3 mg/kg every 8 weeks have better efficacy with adalimumab 40 mg s.c. eow compared to infliximab 3 mg/kg i.v. every 6 weeks.
Although SLE and RA are correlated with genetic predisposing factors such as human leukocyte antigen (HLA) class II, both diseases and other genetic factors might have contributed to the development of dysregulated lymphocyte activation and autoimmunity. Decoy receptor 3 (DcR3)/TR6 is a secreted protein belonging to the tumor necrosis factor (TNF) receptor family. It binds to Fas ligand (FasL), LIGHT, and TL1A that are all TNF family members. It was noted that soluble or solid phase DcR3-Fc co-stimulated proliferation, lymphokine production and cytotoxicity of mouse and human T cells upon T-cell receptor (TCR) ligation. Recently, the investigators found that the serum level of soluble DcR3 was higher in SLE patients than in healthy control subjects (unpublished data). Taken together, the investigators propose that in autoimmune diseases, such as RA and SLE, activated T cells secrete more DcR3 than non-autoimmune controls, which may, in turn, costimulate T cells further and cause dysregulated lymphocyte activation. With the aim to establish the possible correlation between DcR3 genetic polymorphisms, DcR3 expressions, and autoimmune phenotypes, the investigators offer this proposal. They plan to investigate the single nucleotide polymorphisms (SNPs) in the DcR3 gene. The genetic polymorphisms on the DcR3/TR6 gene and circulating DcR3 level will be compared between RA, SLE and non-autoimmune control subjects.