The pro-inflammatory contributions of leukocytes, particularly macrophages and T cells, to the immunopathogenesis of proliferative forms of glomerulonephritis (GN) have been clearly established by various techniques, including in vivo depletion studies in experimental models. The evidence for an active pro-inflammatory role for intrinsic renal cells in GN has relied on studies demonstrating their production of pro-inflammatory mediators in vitro and during the development of GN. Until recently,the specific in vivo contributions of mediators from intrinsic renal cells to inflammatory injury in GN have proven difficult to define. Utilising ‘chimeric’ mice as a tool, several studies have explored the involvement of intrinsic renal cells via their production of cytokines and other key pro-inflammatory molecules. These studies provide evidence of important functional contributions of intrinsic renal cells to inflammatory injury in GN via their expression of cytokines, cytokine receptors, MHC-II and co-stimulatory molecules. They suggest a sequence of interactions between cytokines from leukocytes and intrinsic renal cells and important contributions of glomerular epithelial cell proliferation to crescent formation.