Researchers at The Ohio State University College of Medicine have discovered that an unusual type of immune cell originating in the gut may significantly worsen rheumatoid arthritis (RA) and possibly other autoimmune diseases. Published in Nature Immunology on April 30, the study builds on earlier findings and uncovers how T follicular helper 17 (TFH17) cells—a hybrid of two T helper cell types—are formed in the small intestine’s Peyer’s patches due to stimulation by typically harmless segmented filamentous bacteria (SFB).
Unlike traditional T cells that remain in lymphoid tissues, these TFH17 cells can travel throughout the body and potently stimulate B cells, thereby fueling inflammation and autoimmune responses. Using mouse models, the team traced these cells’ journey from the gut to inflamed joints, demonstrating their pivotal role in disease severity.
Key findings include:
TFH17 cells originate from TH17 cells in the gut and are reprogrammed in Peyer’s patches.
These cells enhance RA symptoms: mice with just 20% of these aberrant cells showed a 4.8-fold increase in arthritis severity.
Gene expression profiling revealed significant overlap between these cells in mice and human RA patients, indicating potential clinical relevance.
This research emphasizes the systemic impact of gut immune responses, especially T cell plasticity, in triggering and worsening autoimmune diseases. Researchers hope future therapies might target these TFH17 cells not only for RA, but for other autoimmune conditions like lupus.
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