Abstract

The primary role of the T-cell system in immune-complex glomerulonephritis induced by intravenous weekly injections of human serum albumin (HSA) in rats has been demonstrated. The development of histological, ultrastructural and immunological glomerular alterations which are clearly recognizable in intact animals was prevented by neonatal thymectomy. In vitro tests of cellular immunity (LIF and PHA responsiveness) revealed a close relationship between the involvement of functioning T-cell subpopulations (at least T-helper) and the development of the classic glomerulonephritic pattern. In other words HSA antigen recognition by T lymphocytes, their cooperation with B lymphocytes, and the activation of the latter with related antibody response represent the immunological sequence which leads to the formation of the soluble circulating immune-complexes responsible for the glomerular injury. Our findings suggest that the same immunological sequence can represent the pathogenetic basis for many forms of glomerulonephritis in which T-dependent antigen stimulation is demonstrable. Our data are also discussed in the light of results obtained by others in immuneglomerulonephritis induced in nude athymic mice.

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