Treating rheumatoid arthritis is difficult because many of the treatments have negative side effects. But now new research could lead to better options.
A study from the University of Birmingham identified cell types called, synovial fibroblasts (SF), which can cause damage to joints typical of rheumatoid arthritis. Researchers could use this information to develop treatments targeted at those cells.
SF cells are a component of the synovium--the connective tissue around human joints. In a patient with rheumatoid arthritis, the SF cells cause damage to the joints by attacking cartilage and bone.
"This study not only shows the existence of distinct sub-sets of synovial fibroblasts, but also suggests that these cells are able to self-organize into lining and sub-lining layers in the presence of cartilage," study leader Adam Croft, MD, PhD, said in a press release. "Combined with the difference in migration rates between the two types of cell, these results are extremely promising in terms of finding new therapeutic targets for treatment of rheumatoid arthritis."
Dr. Croft is a rheumatologist and post-doctoral fellow at the Institute of Inflammation and Ageing at the University of Birmingham.
Dr. Croft and his colleagues identified two distinct types of SF cells, called PDPN and CD248. They discovered that the PDPN type is responsible for causing cartilage damage in people with rheumatoid arthritis.
The researchers grew SF cells from rheumatoid arthritis patients in the lab and inserted them into mice along with human cartilage that simulated a joint.
Examination showed the simulated joint lining contained the invasive PDPN cells. The researchers also found the cells could be activated by the immune system to travel through blood vessels and attack other cartilage in the body. PDPN cells were the first of the two cell types to migrate.
Since rheumatoid arthritis is a disease in which the immune system mistakenly attacks body tissue, current treatment consists of immunosuppressive medications. These medications have serious side effects and can make the patient vulnerable to infections.
The new study indicates that treatment might be targeted to the PDPN cells and cause fewer side effects for patients.
The study was published in the Nov. issue of Arthritis Research and Therapy.
Funding for the study was provided by a grant from Arthritis Research UK.
None of the authors reported a conflict of interest.