T lymphocytes have been implicated in the pathogenesis of inflammatory arthritis for approximately 30 years. Over that period a vast literature has described the phenotype, location and behaviour of T cells derived from patients with inflammatory rheumatological disease. The arthritiogenic roles of MHC class I and class II molecules, which present antigen to T cells, have been hotly debated. The T cell has been variously conceived as a central or peripheral (or even incidental) component in the arthritogenic response. Rapid developments in genomics and use of biological therapeutic agents coupled with recent insights in the field of T cell differentiation and immunoregulation together offer novel methods of investigating the pathogenesis of chronic inflammatory disease. A number of UK researchers, with diverse interests within the field of synovitis, met recently at the Kennedy Institute of Rheumatology. Presentations on T cell memory, cytokines of homeostasis and inflammation, unconventional behaviour of MHC molecules and immunoregulation in murine models, rheumatoid and spondyloarthritis reflected the breadth of the discussion.