Dissecting autoimmunity – B and T cell responses in Rheumatoid Arthritis
Rheumatoid Arthritis (RA) is a complex and heterogeneous inflammatory disorder, where many patients (but not all) display clear autoimmune features characterized by MHC class II association and autoantibody production. Disease develops gradually during a long time period with different compartments being the site of initiation (lung) versus disease precipitation (joints). A functional understanding of this stepwise process is emerging.
We study B and T cells and their effector functions in blood, joints and lungs of RA patients. We utilize peptide – HLA-DR-tetramers as well as antigen-tetramers (for specific T and B cell capture respectively).
Expression of recombinant IgG (BCR) from RA-derived B cells has e.g. revealed an inflammation-independent, but autoimmune, mechanism for pain and bone erosion, explaining some of the conundrums of early aggressive disease.
The possibility to capture antigen-specific lymphocytes is currently applied for immunosurveillance of the autoimmune lymphocyte repertoire in RA patients over time and in response to therapeutic intervention.
2 February 2016, 16:00 (Tuesday, 3rd week, Hilary 2016)
Kennedy Institute of Rheumatology, Headington OX3 7FY
Bernard Sunley Lecture Theatre
Vivianne Malstrom, Professor in Rheumatological Immunology (Dept of Medicine, Center for Molecular Medicine Karolinska Institutet, Stockholm, Sweden)
Kennedy Institute of Rheumatology
Jo Silva (NDORMS),
Wulf Forrester-Barker (University of Oxford, Nuffield Dept of Orthopaedics Rheumatology and Musculoskeletal Sciences),
Gintare Kolesnikovaite (Kennedy Institute of Rheumatology)
Organiser contact email address:
Prof Fiona Powrie (PROFESSOR OF MUSCULOSKELETAL SCIENCES AND DIRECTOR OF THE KENNEDY INSTITUTE)
Kennedy Institute Seminars
Members of the University only