Emily Toulson

• BSc (Hons) Biochemistry
• The role of Bcl-3 as a ‘master’ regulator of T-cell function in the pathogenesis of rheumatoid arthritis

Rheumatoid arthritis (RA) is disease in which a particular type of immune cell called a CD4+ T “helper” cell is thought to “misbehave” to cause autoimmunity – where “friendly fire” by the immune system damages the body. As a result RA patients suffer painful inflammation of the joints and irreversible joint damage. It has been found that a gene called BCL-3 is “switched on” in circulating T helper-cells of early RA patients. We hypothesise that the resultant high levels of BCL-3 protein could be responsible for causing these cells to misbehave, acting as a ‘master regulator’ of T helper cell dysregulation. The aims of this project were to establish whether the over-production of BCL-3 has protective properties over the death (apoptosis) of T helper-cells and whether it results in increased production of interleukin 2 (IL-2) a signalling molecule produced by T-cells when activated by a pathogenic body, such as a microbial infection. These experiments could potentially identify BCL-3 as an important target for future RA treatments that might switch off the irreversible consequences of T helper cell misbehaviour.

Funding source: Newcastle University

Project Supervisors: Noushin Cooper, Oliver Eltherington, Amy Anderson & Professor Dr Arthur G Pratt