T-CELL SUBSETS IN IMMUNOLOGICALLY-MEDIATED GLOMERULONEPHRITIS

Until recently, research on the pathogenesis of glomerulonephritis has been mainly focused on the characterization of humoral immune respons es in the initiation of glomerular injury. However, there is a growing recognition that both cellular and humoral immune responses, in varyi ng proportions, are involved in the pathogenesis of immunologically-me diated glomerulonephritis. T lymphocytes are essential cellular elemen ts of cell-mediated immunity. Both in experimental models of immune-me diated renal disease and in histopathological analyses of human nephro pathies, the involvement of T cells has been demonstrated in the immun oregulation of nephritogenic immune responses and in the immune injury in the kidney. T cell activation resulting in either delayed-type hyp ersensitivity, cytolytic reactions, abnormal expression of major histo compatibility complex (MHC) molecules, or B cell activation can result in glomerulonephritis. These different types of responses are exerted by distinct T cell subsets defined by cell surface markers and cytoki ne profiles. CD4(+) T cells in vivo are functionally heterogeneous wit h respect to cytokine production and the CD45 isoforms that are found on their surface. Like CD4(+) T cells, CD8(+) T cells may also be hete rogeneous at the level of cytokine production. The roles of CD4(+) and CD8(+) cells and their cytokine profiles in glomerulonephritis have n ot been extensively investigated yet, but such studies might improve t he understanding of the pathogenesis and possibly lead to new therapeu tic approaches of human glomerulonephritis. In this review the role of distinct T lymphocyte subsets in experimental and human glomeruloneph ritis will be discussed.