The Foundation funds locally based research projects on the causes and treatments of different forms of arthritis. This includes funding of researchers' salaries, research equipment and the research laboratory, and funding for supporting activities, such as presenting research findings at national and international meetings. Our work contributes to the understanding of arthritis and its treatment as part of the international research community. Work funded by the Haywood Foundation has been published on over 200 scientific papers in international journals.
One of the current research projects underway at the Haywood Rheumatology Centre, through funding provided by the Haywood Foundation, focuses on the role of epigenetic factors (factors which cause changes to the DNA/genes) in the development of rheumatoid arthritis (RA). This is a chronic disease of the joints in which the immune system attacks the joints causing inflammation and damage, leading to functional impairment and disability.
The key aims of this work are to:
1) Identify epigenetic factors that contribute to the development of joint disease in patients with RA; and
2) Investigate whether these new factors might be used to help predict which patients will respond to treatment.
To do this, we are exploiting recent advances in technology that allow us to examine the DNA of patients on a much larger, 'genome-wide' scale - whereas previous methods allowed us to study a single gene at a time, we are now able to analyse more than 20,000 genes simultaneously. Furthermore, and in contrast with other studies that have examined DNA derived from all of the cells in blood together, we are taking a unique approach and looking at individual types of cell that are important in this disease. This includes different types of white blood cell (T-cells and B-cells), and also a type of cell from the joint itself (fibroblasts). With this approach, and for the first time, we have discovered previously unknown disease-specific changes to the DNA in T-cells and B-cells from patients with RA. We have also identified similar changes in fibroblast cells from the joint in these patients. Identification of these new targets contributed to a better understanding of the factors involved in joint inflammation and damage, and will be important for the development of new therapies to treat the disease.
Using these methods we are also studying whether changes to the DNA in T-cells and B-cells can be used to 'predict' the likely treatment response in newly diagnosed patients with RA. The ability to identify at diagnosis which patients are likely to respond to treatment will be a highly significant advancement for improved clinical management of this disease and would have direct patient benefits, for example through the targeted use of treatments that are most likely to be effective (and the earlier use of alternative therapies in those patients who are less likely to respond to standard treatments).