12pm, Tuesday 21 February, Seminar Room 1, Level 2, TRF
Thesis title: GILZ regulates type 1 IFN production in SLE and represents an effective, metabolically inert alternative to GCs for the treatment of SLE.
Synopsis: Systemic lupus erythematosus (SLE) is a clinically diverse autoimmune disease characterized by the loss of tolerance to nuclear self-antigens and autoantibody production, and type 1 Interferon play a critical role in SLE pathogenesis. The majority of patients with SLE are typically treated with Glucocorticoids (GCs) due to their broad anti-inflammatory effect but result in significant metabolic adverse effects that contribute to increased morbidity and mortality in SLE.There is a critical need for alternative therapies to glucocorticoids that can exert similar anti-inflammatory effects, such as inhibition of type I interferon production, but without causing the metabolic adverse effects of GC. GILZ (Glucocorticoid-induced leucine zipper), a GC-inducible protein, may represent such an alternative. Thus, I aim to determine that GILZ regulates type 1 IFN production and is metabolically inert distinct from GCs. This work will validate GILZ as a therapeutic target in SLE and potentially lead to a therapy reducing dependence on GC in SLE treatment.
Supervisors: Prof Eric Morand, Dr Sarah Jones and Prof Michelle Leech
Panel Chair: Dr George Grigoriadis
Independent assessors: Dr Alberta Hoi, Prof Philip Hodgkin