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.