The MRL-Ipr/Ipr Mouse. A Model for the Study of Rheumatoid Arthritis

Abstract

Autoimmune MRL-lpr/lpr 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-lpr/lpr 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-lpr/lpr 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-lpr/lpr mice. Although the mechanisms underlying cartilage injury in MRL-lpr/lpr 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-lpr/lpr mice may provide important insights concerning the pathogenesis of rheumatoid arthritis.