To investigate the role of interleukin-1 beta (IL-1 beta) in glomerulonephritis we studied the presence of IL-1 beta by in-situ hybridization in in-situ immune complex glomerulonephritis in the rat. Glomerulonephritis was induced in preimmunized rats by unilateral renal perfusion with cationized human IgG. In-situ hybridization was performed on frozen sections with a battery of four 30mer oligonucleotide DNA probes 3' end labelled with 35S-dATP. IL-1 beta mRNA was detectable in nephritic glomeruli at 6 and 24 hours after induction of glomerulonephritis. Signal was maximal at 48 hours and markedly reduced by 4 days. The peak of IL-1 beta transcription coincided with the major monocyte influx into glomeruli consistent with a role for IL-1 beta as a mediator of glomerular hypercellularity.