What is it about?
A team of researchers has uncovered a unique type of lymphocyte in rheumatoid arthritis (RA), a chronic, painful joint disease that affects millions worldwide. Their study reveals that a small group of immune cells, called CD74+ T cells, may be key drivers of joint inflammation and disease flare-ups in RA. This research shows that when MIF or its receptor, CD74, is missing in mouse T cells, the animals don’t develop joint inflammation. Even more intriguing, the researchers found that these CD74+ T cells multiply during arthritis and can trigger the disease if transferred to healthy mice. The team also discovered these CD74+ T cells in the blood and joints of people with RA, suggesting the findings are highly relevant to human disease. By blocking the MIF/CD74 pathway, it might be possible to prevent recurrences of joint inflammation, which occur commonly, offering hope for new treatments, especially for patients who don’t respond to current therapies.
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Why is it important?
This study shines a spotlight on a previously overlooked group of immune cells (CD74+ T cells) and opens the door to innovative therapeutic targets that could one day help people with RA live free of painful disease flares.
Perspectives
The identification of a new subset of T cells and their critical role in RA pathogenesis is exciting. CD74 T cells offer a new avenue for us to look for long-term remission of RA hopefully preventing further joint damage over a person’s life. Beyond this study, we are investigating CD74 T cells in other autoimmune diseases and in cancer.
Edward Doherty
Yale University
Read the Original
This page is a summary of: Pathogenic role of MIF receptor (CD74) expressing T cells in inflammatory arthritis, Proceedings of the National Academy of Sciences, January 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2509156123.
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