We attempted to identify a clonal proliferation of T cells from synovial fluid samples from patients with rheumatoid arthritis, using techniques of restriction fragment length polymorphism. We used probes for the Rheumatoid arthritis (RA) is thought to develop as a consequence of disordered immune regulation in a genetically susceptible host (1). Although no inciting agent has been detected, evidence has accumulated implicating an infectious etiology-possibly viral. Moreover, data support the concept of a local hyperimmune state within the synovial tissues and suggest at least the possibility of a sequestered antigen driving