The Use of Biologic Therapies to Induce New Populations of Treg in Autoimmunity
Status: This talk is in preparation - details may change
Limiting the severity of inflammation and its eventual resolution are critical pathways which are vital to minimizing damage to host tissues. We study the ability of the biologics otelixizumab (anti-CD3) and adalimumab (anti-TNF) to induce a potent CD8+FOXP3+ regulatory T cell (Treg) population in rheumatoid arthritis patients. These Treg can suppress CD4+ T cell proliferation and IL-17 and IFN-γ production; however their mechanism of action is unknown. We have been studying how monocytes are crucial for the induction of FOXP3 expression in CD8+ T cells and how CD8+ T cells can control their ability to become a Treg via p38 phosphorylation.

Our studies aim to 1) identify novel therapeutic targets that may mimic Treg function or 2) enhance the efficacy of biologic drugs used in the clinic to treat RA and type 1 diabetes by the use of combination therapy.
Date: 15 June 2015, 12:00 (Monday, 8th week, Trinity 2015)
Venue: Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details: Bernard Sunley Lecture Theatre
Speaker: Dr Clare Notley (Centre for Rheumatology, University College London, London )
Organising department: Kennedy Institute of Rheumatology
Organisers: Professor Irina Udalova (Kennedy Institute of Rheumatology), Professor Kim Midwood (Kennedy Institute of Rheumatology)
Organiser contact email address: sandra.lock@kennedy.ox.ac.uk
Host: Dr Fiona McCann (Kennedy Institute of Rheumatology)
Part of: Kennedy Institute Seminars
Booking required?: Not required
Audience: Members of the University only
Editor: Sandra Lock