Rheumatoid Arthritis (RA) is a common and chronic autoimmune disease that causes erosive joint damage and deformities with increased risk for disability and reduced life expectancy. Current therapies have significantly improved disease control but remission is still rare.
The Gulko Lab work focuses on discovering new genes implicated in (RA), identifying prognostic biomarkers and generating new targets and more effective therapies to cure RA and other autoimmune diseases. Over the past twenty years Dr Gulko and his team have published a number of studies demonstrating the importance of modulating severity and destruction of RA. We believe that new and more effective therapies will emerge from better understanding the process implicated in the regulation of disease severity and joint damage in RA.
RA can be distinguished from other inflammatory conditions of the joints because of the presence of unique cells, the Fibroblast-like synoviocytes (FLS) that like cancer cells invade and destroy the cartilage and bones and contribute significantly to the perpetuation of the disease. FLS in RA show alterations in their invasive behavior. The Gulko lab published the first study providing evidence that the invasive properties of FLS are genetically regulated.
Our long-term goals are to identify the mechanism underlying rheumatoid arthritis pathogenesis, with particular emphasis on understanding the events taking place in the synovial tissue. A major focus of our work has been to understand the abnormal and cancer-like behavior of the synovial fibroblast in RA as this cell is central to bringing inflammatory cells into the synovial tissue and mediate joint damage and erosive changes. Our studies are directed toward the identification of new genes and development of new and more effective therapies and prognostic biomarkers.