Autoimmune MRL-Ipr/Ipr mice develop a spontaneous destructive arthropathy sharing some features with rheumatoid arthritis including synovial cell proliferation, pannus formation, rheumatoid nodule-like lesions and circulating rheumatoid factors. Rheumatoid factors elaborated by MRL-Ipr/Ipr mice exhibit binding characteristics similar to those found in the sera of patients with rheumatoid arthritis; however, these autoantibodies do not appear to be essential for the induction of arthritis in MRL-Ipr/Ipr mice. Molecular studies, indicating that VH genes from several VH families are capable of encoding these rheumatoid factors, argue against the existence of unique "autoantibody genes" in the germline of MRL-Ipr/Ipr mice. Although the mechanisms underlying cartilage injury in MRL-Ipr/Ipr mice have not been elucidated, available evidence suggests that invading synovial cells play an important role. Delineation of the cellular and molecular mechanisms responsible for articular destruction in MRL-Ipr/Ipr mice may provide important insights concerning the pathogenesis of rheumatoid arthritis. © 1988 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.