For many decades it has been known that there are variable degrees of interstitial infiltration of leukocytes in the majority of experimental and human glomerulonephritides [1-5]. The pathogenetic mechanism that triggers this inflammatory reaction and the possible role it may play in the progression of immunologically mediated glomerular diseases have been long debated, and there are great differences in opinion.

Very recently technology has become available for marking the extrinsic cells infiltrating renal interstitium with monoclonal antibodies that recognise specific cellsurface antigens. This has made possible a more precise quantitative evaluation and phenotypic characterisation of these cells, and has revealed an abnormal discrete diffuse infiltration of leukocytes, including T-lymphocytes and sometimes also monocy tes, even in the renal tissue of some glomerulonephritic patients for whom the traditional staining techniques had not disclosed any significant infiltration. The characterisation of such extrinsic cells has shed more light on the immunological mechanisms that may be responsible for the tubulointerstitial damage in immunologically mediated glomerular diseases. We will briefly analyse the most recent data obtained with this new technology.