Rheumatoid arthritis (RA) is an autoimmune disease that affects millions worldwide and can have a devastating impact on patients’ lives. Yet, about one in three patients respond poorly to existing treatments. Researchers at Kyoto University have shed new light on this challenge by discovering that peripheral helper T cells (Tph cells), a key type of immune cell involved in RA, exist in two forms: stem-like Tph cells and effector Tph cells. The stem-like Tph cells reside in immune “hubs” called tertiary lymphoid structures within inflamed joints, where they multiply and activate B cells. Some of these then become effector Tph cells that leave the hubs and cause inflammation. This continuous supply of effector Tph cells may explain why inflammation persists in some patients despite treatment. Targeting the stem-like Tph cells at the source could offer a new therapeutic strategy, bringing hope for more effective symptom relief and improved quality of life for patients living with RA.

This research is led by Yuki Masuo, a doctoral student at the Graduate School of Medicine, Kyoto University; Associate Professor Hiroyuki Yoshitomi of the Department of Immunology (also Associate Investigator at WPI-ASHBi), Graduate School of Medicine, Kyoto University; and Professor Hideki Ueno, Vice Director and Principal Investigator at WPI-ASHBi (also Professor at the Department of Immunology, Graduate School of Medicine, Kyoto University, and Director of the Kyoto University Immunological Monitoring Center, KIC). These findings will be published online in Science Immunology on August 15, 2025, at 2:00 PM local time (August 16 at 3:00 AM JST).

Researchers at Kyoto University have discovered that an immune molecule found only in primates, called IGFL2, plays a key role in regulating inflammation in rheumatoid arthritis (RA). IGFL2 is produced by a subset of immune cells in the joints of patients with RA and acts like fuel on a fire: it activates more immune cells, further amplifying inflammation and worsening joint damage. They also found that IGFL2 levels were much higher in the blood of patients with RA, especially in those with more severe symptoms. These findings support IGFL2’s potential as a diagnostic marker, a tool for monitoring disease progression, and a target for new therapies, paving the way for earlier detection, more effective treatments, and better quality of life for people with RA worldwide.

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