SLE genetics: overview and an example of disease mechanism
Systemic lupus erythematosus (SLE) is a generalised autoimmune disease that can affect virtually any organ/tissue. It exhibits marked sexual dimorphism, being ten times more prevalent in females; it is also more common in non-European populations. Genome-wide association studies have mapped approximately 80 risk loci that implicate a range of cells in both the innate and adaptive immune systems. The disease heterogeneity remains to be explained, however, our preliminary analyses suggest that genetic risk operates in a quantitative rather than qualitative manner. I will finally take one example of an SLE risk locus (TNFSF4) that encodes the lymphocyte costimulatory molecule OX40L. I will outline, how transancestral analysis, gene expression studies and the use of mouse models support a cellular mechanism through which the genetic risk alleles predispose to SLE.
Date: 8 February 2018, 16:00 (Thursday, 4th week, Hilary 2018)
Venue: Wellcome Trust Centre for Human Genetics, Headington OX3 7BN
Venue Details: Rooms A&B
Speaker: Professor Tim Vyse (King’s College London)
Organising department: Wellcome Trust Centre for Human Genetics
Organiser: Isabel Schmidt (University of Oxford, Wellcome Centre for Human Genetics)
Part of: WHG High Profile Seminars
Booking required?: Not required
Audience: Members of the University only
Editor: Isabel Schmidt