The immunopathogenesis of rheumatoid arthritis is discussed in two ways. First, we consider the major question of whether T cells are likely to drive the disease. Second--and assuming T cells to be important--we discuss available data on the components of the trimolecular complex (major histocompatibility complex class II-antigen-T-cell receptor), which are possibly involved in the disease. Our two main points are that the most important questions concerning the pathogenesis of rheumatoid arthritis require answers from immunointervention in patients, and that animal experiments can be increasingly used in interpreting current experiments in humans.