Targeting early changes in the synovial microenvironment could offer a new class of rheumatoid arthritis therapy, finds a study carried out by the Universities of Birmingham and Oxford.
Patients with conditions such rheumatoid arthritis experience pain, swelling and stiffness in the joints due to inflammation in the joint lining which can eventually destroy joints. These inflamed joints are heavily infiltrated by activated immune cells which drive joint swelling and joint destruction. This study addresses some of the mechanisms which drive the activation of these immune cells.
Importantly, it shows that a component of the tissue between the immune cells in the joint lining – specifically a component of the extracellular matrix protein tenascin-C – is responsible for some of this activation. By treating either immune cells in culture, or an in vivo model of arthritis, with a drug that blocks tenascin-C, immune cell activation and arthritis activity were reduced.
The collaborative research, published in Annals of the Rheumatic Diseases, was led by Professor Kim Midwood from Oxford University and involved collaborators from Cambridge-based companies IONTAS and Nascient Ltd.
Professor Karim Raza, Arthritis Research UK Professor of Rheumatology from the Institute of Inflammation and Ageing, explained: “The work so far is at an early stage. Moving forward we look forward to collaborating with Professor Midwood to develop approaches to testing whether this strategy works in patients with arthritis with a view to developing a new type of drug which could be used in clinical practice.”
This work was funded by grants from Nascient Ltd, Arthritis Research UK and the Kennedy Trust for Rheumatology Research and was supported by the National Institute for Health Research (NIHR)/Wellcome Trust Clinical Research Facility at University Hospitals Birmingham NHS Foundation Trust and the NIHR Birmingham Biomedical Research Centre.