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
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