Dr. Guang-Sheng Ling
Centre for Inflammatory Disease, Department of Medicine
Imperial College London, UK

Date: Tuesday, 26-February-2019
Time: 11:00 a.m.
Venue: Seminar Room 3-38, 3/F, Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Pokfulam, Hong Kong

Summary:
Complement protein C1q deficiency is the strongest risk factor known for the development of Systemic lupus erythematosus (SLE). While the removal of apoptotic debris is implicated in C1q-mediated protection against SLE, there are several redundant clearance pathways. The pleiotropic nature of C1q also suggests it can promote immune tolerance via alternative mechanisms. Our recent study shows that C1q functions as a metabolic regulator of CD8+T cells and restrains their pathogenic responses during autoimmunity and viral infections. Our findings describe a new paradigm to explain how C1q may prevent lupus flares after infection and propose novel concept placing metabolic dysregulation of CD8+T cells at the forefront of SLE pathogenesis.

ALL ARE WELCOME