Genetic and epigenetic activation of fibroblasts in rheumatoid arthritis


Synovial fibroblasts are the major resident cells of the synovium and play a central role in joint inflammation in rheumatoid arthritis (RA). They are characterized by a stably activated invasive phenotype that is maintained in cell culture. We and others have shown that epigenetic alterations, such as changes in DNA methylation, occur in RA synovial fibroblasts and may underlie this aggressive phenotype. Recently, we have shown that genetic factors also play an important role in fibroblast activation in RA. We have created a comprehensive chromatin map of synovial fibroblasts, which allowed us to reveal the functional significance of RA risk SNPs in synovial fibroblasts. This allowed us to identify several novel pathways that may drive synovial fibroblast activation in RA, some of which may explain the pathognomonic involvement of the small distal joints in RA.

From 21 Jun 2024 11:30
Until 21 Jun 2024 12:30
Location FSVMII building, seminar room, L5

Speaker Caroline Ospelt
Affiliation Department of Rheumatology, University Hospital of Zurich, University of Zurich, Switzerland
Host Dirk Elewaut

About the speaker

Caroline Ospelt completed her medical studies at the Leopold-Franzens-University Innsbruck (Austria) and her PhD at the University of Amsterdam (The Netherlands). She received the venia legendi (lecturer) from the University of Zurich in 2014 and has since been group leader at the Center for Experimental Rheumatology, University Hospital of Zurich, Switzerland. In 2020, she was appointed Professor ad Personam of Experimental Rheumatology. Her research focuses on genetic and epigenetic alterations and joint-specific functions in synovial fibroblasts from patients with rheumatoid arthritis. She has authored more than 100 peer-reviewed publications, has served on scientific committees of several international congresses and panels, and is an editorial board member and social media advisor for Annals of the Rheumatic Diseases and RMDopen.