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Dear All,
Greetings of the day!
Highlight of this issue is a study, “Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis,” by Gareth W. Jones and his team, which is published in the Journal of Experimental Medicine. Gareth W. Jones and his team discovered that cytokine interleukin-27 (IL-27) inhibits formation of ectopic lymphoid-like structures (ELS) in patients with rheumatoid arthritis (RA), thereby preventing ELS to contribute to disease progression through recruitment and maturation of inflammatory cells to inflamed tissues. In a subset of RA patients (approximately 40%), inflamed joints develop ELS that contribute to the disease pathology. Specifically, these aggregates are associated with disease severity, activation of key immune cells (T cells and B cells) and autoantibody production.
In this study, authors investigated the role of IL-27 in RA synovial pathology. The team used mice deficient for the Il27ra gene (encoding IL-27 receptor α chain), used as a model for antigen-induced arthritis, observing that these mice exhibited more severe RA when compared with wild-type (that express the functional Il27ra gene) controls. In Il27ra-deficient mice, researchers observed increased expression of proinflammatory cytokines in mice synovium, hypertrophy, and both cartilage and bone degradation. In agreement with IL-27 controlling T helper 17 responses, the team observed that knock-out mice for IL-27 had higher levels of the cytokine expressed in inflamed synovium.
These findings were further validated in RA patients’ synovial tissues, where they found that low levels of IL-27 increased the incidence of ELS. Additionally, IL-27 levels and infiltration of inflammatory T cells (CD3+ and CD20+ cells) and synovitis were inversely correlated: low IL-27 levels promoted inflammation.
These data suggest IL-27 may negatively regulate the occurrence of ELS in RA patients, and the authors propose that measuring IL-27 levels in this population of patients can potentially be used as a biomarker for diffuse synovial histopathology and a potential target for future therapeutic interventions in RA.
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Regards,
Banwari Sharma
Editor, IRA e-Newsletter
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