Type-1 interferon response in metabolic inflammation and cellular bioenergetics
Metabolic inflammation in type-2 diabetes (T2D) is initiated by type-1 interferon signalling, through its transcriptional mediator IRF5. Whilst studies in auto-immunity link pro-inflammatory polarisation to increased glycolysis, this phenomenon remains unexplored in T2D or in the context of IRF5-dependent inflammation. We hypothesise that macrophage bioenergetic adaptation in T2D is distinct, due to the distinct nature of insult and systemic abundance of substrates. IRF5 may play a key role in adapting cellular bioenergetics to initiate, amplify and sustain inflammation. To address these hypotheses, we analysed public and in-house sequencing datasets and carried out mechanistic in vivo and ex vivo analyses.
Date: 4 November 2019, 12:00 (Monday, 4th week, Michaelmas 2019)
Venue: Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details: Bernard Sunley Lecture Theatre
Speaker: Dr Fawaz Alzaid (Paris’ Cordeliers Research Centre, France)
Organising department: Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS)
Organiser: Jennifer Pope (Kennedy Institute of Rheumatology)
Organiser contact email address: jennifer.pope@kennedy.ox.ac.uk
Host: Professor Irina Udalova (Kennedy Institute of Rheumatology)
Part of: Kennedy Institute Seminars
Booking required?: Not required
Audience: Public
Editor: Jennifer Pope