Although autoantibodes and autoantibody-producing B cells are crucial for the initiation of lupus nephritis, their precise role in the development of the nephritic lesions is incompletely understood. This article summarizes the results of recent work in our laboratory related to this area. They indicate that not all autoantibodies are pathogenic. Furthermore, among the pathogenic subset, individual immunoglobulins produce clearly distinguishable immune deposit patterns in specific glomerular locations and this is associated with different disease profiles (i.e., inflammation, proteinuria). The variation in immune deposit formation induced by the individual autoantibodies are reminiscent of the different lesions in lupus patients, and they appear to be related to differences in the reactivity of autoantibodies with specific glomerular antigens. Thus, it appears that the predominant interaction in a given individual influences the morphologic and clinical expression of disease. Autoantibody-producing B cells also influence the activation of autoreactive T cells that infiltrate the kidney to produce vasculitis and interstitial nephritis, and the potential mechanisms responsible for this phenomenon are discussed.