Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Monday, 8 June 2026, 12pm to 1pm

Chronic inflammation in autoimmune disease reflects a failure to resolve immune responses despite the presence of tissue-repair programs. Emerging evidence points to metabolic checkpoints as key determinants of immune cell fate, linking cellular bioenergetics to inflammatory function and survival. In rheumatoid arthritis, reparative macrophages undergo a metabolic shift driven by autocrine C1q signaling, leading to activation of the NAD⁺ hydrolase SARM1. This results in NAD⁺ depletion, mitochondrial crisis, and accumulation of cyclic ADP ribose, which triggers PANoptotic cell death. The resulting lytic death amplifies tissue inflammation, identifying SARM1-dependent metabolic collapse as a mechanism sustaining chronic autoimmune pathology and a potential therapeutic target.

Speaker(s): Prof. Cornelia Weyand (Mayo Clinic College of Medicine and Science and the Mayo Clinic Alix School of Medicine)

Venue: Kennedy Institute of Rheumatology - Kennedy Lecture Theatre - Kennedy Lecture Theatre Kennedy Institute of Rheumatology Headington Oxford Oxfordshire OX3 7FY United Kingdom

Department: Kennedy Institute of Rheumatology (Unit)

Organiser: Tess Lawless

Host: Professor Christopher Buckley