UCL investigators have identified a new mechanism which may explain the occurrence of rheumatoid arthritis, the second most common type of arthritis in the UK.
The research, carried out at UCL by Professor Claudia Mauri and her team and published in Science Translational Medicine, discovered that in patients with active rheumatoid arthritis the number of regulatory B cells circulating in the blood is reduced, and these B cells do not function efficiently enough to prevent autoimmune responses and inflammation.
Professor Mauri works within Rheumatology at UCL; where the III Programme provides infrastructure support for clinical studies via research nurse capacity.
Rheumatoid arthritis is an autoimmune disease which means the body's immune system mistakenly attacks the healthy tissue of the synovium, a thin membrane that lines the joints. This leads to inflammation of the joints and surrounding tissues which can be very painful and often disabling. Although it is a result of autoimmunity, the trigger itself of rheumatoid arthritis is still unknown.
This study concludes that treatments that increase the number of regulatory B cells, and restore their normal functions, could benefit patients.
Professor Mauri explains: “Key cells in the immune system are ‘B cells’ and ‘T cells’, each of which represents a family of ‘sub-sets’, which have slightly differing behaviors in the inflammation pathway. One of these subsets ‘regulatory T cells’ has been associated with the protection of autoimmune diseases for some time and has been previously shown that they fail to work properly in patients with autoimmunity. In this paper, we have shown, for the first time, that the number and function of ‘regulatory B cells’ is also abnormal in patients with rheumatoid arthritis.”
The research was published in Science Transitional Medicine on 20 February 2013: Vol. 5, Issue 173, p. 173ra23.
