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Genetics, Viruses, and B cells: the Cause of Multiple Sclerosis
In-person only
A pipeline was developed to quantify EBV DNA from whole-genome sequencing data in a cohort of over half million subjects identifying 39 susceptibility risk loci. A significant overlap with genetic variants associated with MS risk was observed p<10-12. These data suggest that EBV-infected B cells may constituted a critical hub that modulates T cell responses while activating MS gene linked susceptibility pathways within B cells. Finally, B cell depletion is almost totally effective in stopping autoimmune MS. Thus, we define a genetic and cellular framework linking B cells to the initiation of MS and support a causal role of EBV activity on MS risk.
Date:
19 February 2026, 12:00
Venue:
Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details:
Kennedy Lecture Theatre
Speaker:
Professor David Hafler (Yale School of Medicine)
Organising department:
Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS)
Organisers:
Tess Lawless (Kennedy Institute of Rheumatology),
Katie Roberts (University of Oxford)
Host:
Prof Dame Fiona Powrie (The Kennedy Institute of Rheumatology)
Part of:
Kennedy Institute Seminars
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Katie Roberts
