Analysis of Synovial Fluid and Peripheral Blood Samples from Patients with Rheumatoid Arthritis and Using Patients with Osteoarthritis as Controls

Summary Better understanding of the pathophysiology of Rheumatoid arthritis (RA) has led to the development of new therapeutic strategies. Despite this there is still an unmet need with an important number of patients not achieving low disease states or remission.

Project Details

Granulocyte macrophage-colony stimulating factor (GM-CSF) has been found to be a key mediator in inflammation and autoimmunity, and is seen as a novel target for treatment in RA. The downstream effects of GM-CSF blockade still need to be better delineated. We hypothesize that there is a pro-inflammatory autocrine/paracrine loop involving cytokines like GM-CSF and CCL17 which drives RA and possibly osteoarthritis (OA) pathogenesis. The primary aim of this study is to determine the ability of cytokines like GM-CSF to activate synovial fluid mononuclear cells or blood monocytes from RA and OA patients, and the ability of anti-cytokine antibodies to modulate such activation.

Methods: We are recruiting RA and OA patients with symptomatic swollen joints, who require joint aspiration for diagnostic and/or therapeutic purposes. Mononuclear cells and peripheral blood monocytes are isolated from collected samples and are either left stimulated or unstimulated with cytokines (GM-CSF) in the presence or absence of anti-cytokine antibodies. Inflammatory mediator mRNA expression is then measured using qPCR.