Immune System Proteins Dictate Severity of Rheumatoid Arthritis

An immune system protein called interleukin 27 may be able to prevent the onset of an aggressive form of rheumatoid arthritis (RA), according to findings published in the Journal of Experimental Medicine.

Researchers from Cardiff University set out to understand the regulatory functions of interleukin 27 in the inflammatory process in order to demonstrate that low interleukin 27 expression is linked to increased incidence of ectopic lymphoid-like structures. In ectopic lymphoid-like structures, an especially aggressive form of RA, interleukin 27 causes symptoms such as swollen and painful joints. In the United Kingdom, where the research took place, the study authors mentioned that the ectopic lymphoid-like structures account for up to 40 percent of diagnoses. Plus, an additional 40 percent of patients with the disease do not respond to existing treatment.

The researchers learned that by understanding the process and uses for interleukin 27, they and other investigators will be able to divide RA patients into sub groups based on how the varying patterns of the disease differ. The study authors added that the disease patterns depend on how much interleukin 27 is present in each patient’s joints. A patient’s classification into these subgroups can dictate the appropriate, individualized therapy they will receive. The study authors said that this can aid patients’ abilities to overcome the disease.

The study authors believe that their identification of the role of interleukin 27 in inflammation will jump start the exploration for new therapeutics that would manipulate the pathways that influence interleukin 27.

“In all forms of rheumatoid arthritis, it is widely understood that early intervention offers the best chance for clinical remission,” Dr. Gareth Jones explained in a press release. “The sooner treatment begins, the more effective the therapeutic response is likely to be. The key is identifying which drug is best suited for an individual patient. Making the correct treatment decisions, sufficiently early in the disease process will improve disease outcome, enhance a patients wellbeing and overall quality of life. Our research is identifying crucial pathways and mechanisms that allow us to distinguish between different sub types of RA, using experimental models that mirror human forms of the disease. Agents that manipulate the activities of these pathways may also serve as potential therapies for future development.”

Professor Christopher Buckley, a researcher on the project, underlined the idea that interleukin 27 can help categorize patients with RA into groups, aiding the individualized therapeutic approach.

“Furthermore, identifying interleukin 27 as a bio-marker of the type of RA in which lymphoid tissue forms in the synovium, suggests that targeting this cytokine might be beneficial,” Buckley concluded.