Immunology researchers from the University of Cardiff have identified a mechanism involving interleukin-27 in the inflammatory pathway of rheumatoid arthritis associated with lymphoid tissue formation. The study, funded by Arthritis Research UK and entitled “Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis”, was published in the Journal of Experimental Medicine.
In an effort to predict and prevent the onset of a specific variant of RA, scientists used mice experimental models and synovial tissues from rheumatoid arthritis (RA) patients. Results allowed the team to identify the protein interleukin-27 (IL-27) as a biomarker for specific sub-types of lymphoid-rich RA, which corresponds to about 40% of diagnoses. The results showed that low IL-27 expression corresponds to an increased presence of lymphoid-like structures, which develop at sites of inflammation and cause the swollen painful joints. These results were also observed in mice lacking the IL-27 receptor, further confirming the correlation between IL-27 concentration in patient’s joints and degree of inflammation.
This research may help identify which disease sub-group patients belong to allowing clinicians to decide on a more targeted treatment earlier on the diagnosis stage. Importantly, it can also lead to the identification of a potentially new target for drug development. Professor Christopher Buckley, from the Rheumatology Research Group at the University of Birmingham, highlighted the major consequences of this discovery: “The potential of interleukin-27 as a marker to stratify patients with RA into different groups is a very important discovery that will help transform our ability to use a more personalized approach in the management of patients with the most aggressive form of the disease.”
First author Dr. Gareth Jones, from the School of Medicine’s Institute of Infection & Immunity concluded, “In all forms of rheumatoid arthritis, it is widely understood that early intervention offers the best chance for clinical remission. The sooner treatment begins, the more effective the therapeutic response is likely to be. Making the correct treatment decisions, sufficiently early in the disease process will improve disease outcome, enhance a patients wellbeing and overall quality of life. “
