T lymphocytes play a critical role in the inflammatory process of rheumatoid arthritis (RA). Studies in a new animal model of RA, created by implanting human inflamed synovium into SCID mice, have confirmed that the production of matrix-degrading enzymes and pro-inflammatory cytokines is ultimately under T-cell control. T-cell dysfunction in RA patients also alters T-cell dynamics, resulting in profound abnormalities in T-cell pool composition. The cause and consequences of altered T-cell dynamics in RA are not yet understood, but factors determining T-cell homeostasis include the generation of new T cells, loss of T cells during immune responses and self-renewal of T cells within the system. Understanding the mechanisms that govern the formation of the T-cell pool in RA emphasizes the dynamic and quantitative aspects of lymphocyte behaviour in RA and has profound therapeutic implications when devising strategies to counteract T-cell dysfunction.