The control of inflammatory pain and disease- a new pathway?
In person only
Granulocyte macrophage-colony stimulating factor (GM-CSF) blockade and that of its receptor are effective in inflammatory arthritis models and rheumatoid arthritis trials. We have discovered a GM-CSF/CCL17 pathway in monocytes/macrophages. The putative role of this pathway in both inflammatory arthritis and osteoarthritis (OA) pain and disease, including in obesity-associated OA, will be discussed. Ideas on the mode of action of CCL17, including its possible involvement in fibrosis/fibroblast biology, will also be presented. In contrast to the well-recognized chemotactic role of CCL17 (e.g. preferential Th2 cell chemotaxis), these data reveal a lymphocyte-independent, non-chemotactic and algesic role of CCL17 in arthritis and possibly other indications, and suggest that it could be a potential therapeutic target in inflammatory pain and disease.
Date: 17 April 2024, 12:00 (Wednesday, 0th week, Trinity 2024)
Venue: Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details: Bernard Sunley Lecture Theatre
Speaker: Prof John Hamilton (University of Melbourne)
Organising department: Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS)
Organiser: Doris Chan (Kennedy Institute of Rheumatology)
Organiser contact email address:
Host: Prof Christopher Buckley (University of Oxford)
Part of: Kennedy Institute Seminars
Booking required?: Not required
Audience: Members of the University only
Editor: Doris Chan