Lupus nephritis is a major complication of systemic lupus erythematosus (SLE) and is associated with a high rate of morbidity and mortality. While many different immunologic and nonimmunologic factors contribute to disease expression in lupus nephritis, a large body of evidence suggests that the production of anti-DNA antibodies and the formation of glomerular immune deposits are important initial events in the pathogenesis of the disease. This review will summarize our current understanding of the differences between pathogenic and nonpathogenic autoantibodies, the mechanisms by which these autoantibodies induce renal injury and the effector mechanisms which are subsequently activated by the deposited autoantibodies that ultimately lead to the expression of the different lupus lesions.