Objective
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterised by cartilage and bone erosion. In order to target the joint and the inflammation process specifically, avoiding systemic secondary effects of biological compounds, we have: engineered T cells to recognise collagen type II (CII), a main constituent of cartilage, with a chimeric receptor composed of a scFv extracellular domain which binds to CII and an intracellular domain which signals inducing cytokine production and T cell proliferation; and modified cytokines with a biodegradable 'shell' that is removed in sites of inflammation by MMP activity.