Arthritis is a leading cause of disability that affects up to 15% of the Irish population. 2% suffer from inflammatory arthritis such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Many patients respond poorly, not at all or suffer drug side-effects. We cannot predict who gets RA or PsA, who will progress and what medicine will work. Patients need smart, safe and effective treatments. Activation of inflammation in our immune-cells is a key mechanism by which our body fights infection. However, if uncontrolled, the immune response doesn’t switch off and this contributes to development of autoimmune-diseases including RA and PsA causing joint damage and disability. PsA is also associated skin psoriasis. While common pathogenic features exist between RA and PsA, there are also differences which may explain their distinct clinical features, and more importantly, it may explain different responses to specific therapies, that impact on disease outcomes and prognosis. One of the earliest events in these diseases is the formation of new blood vessel in the joint, which allows immune and inflammatory cells to enter the joint, and cause inflammation. We and others have previously demonstrated differences in the shape of these blood vessel and activation in PsA and RA reflecting both differential pathogenesis and disease outcome, however what drives these differences is unclear. Thus, the current project aims to further investigate what causes the differences in the blood vessels in the PsA and RA joint, specifically their activation, how they move, and their role in attracting immune cells.
