The exact roles played by specific antibody, circulating antigen—antibody complexes and cellular immunity in the causation of experimental glomerulonephritis of rats (EGN) need clarification and a sequential study of these factors was therefore undertaken. Rats immunized with renal tubular antigen and studied for humoral response only (group I) produced neither precipitating nor 2- or 48-hour PCA antibodies but did have an antibody titre by an immunofluorescent test against the proximal portion of the proximal convoluted tubular cells by the second to sixth week post-immunization in six of six animals. A C1q test for antigen—antibody complexes became positive in most rats at the time of onset of proteinuria. Rats in group II were studied for cellular immunity to the renal tubular antigen. Skin tests did not become positive until approximately the time of onset of proteinuria when peripheral blood lymphocyte cultures were also stimulated in seven of nine rats tested. Direct immunofluorescence of the kidneys from this group revealed a linear deposition of γG and renal tubular antigen along the glomerular basement membrane. Since both cellular immunity and antigen—antibody complexes involving the renal tubular antigen were present at the onset of proteinuria, both modalities may play a significant role in EGN.