Local renal graft-versus-host reaction: sequential ultrastructural study.
A sequential study has been made of the ultrastructure of local renal graft-versus-host reactions produced in cyclophosphamide-pretreated rats by injection of either allogeneic or xenogeneic (mouse) spleen cells beneath the renal capsule. Early in the reaction, immunoblasts were seen between the outer cortical tubules, and there was associated interstitial oedema and tubular degeneration. In places, several small lymphocytes were observed clustered around and in close cytoplasmic contact with individual immunoblasts, perhaps representing interaction between donor and host cells. As the reaction proceeded, the number of lymphoid cells increased by immigration from peritubular vessels. Some tubules were invaded by lymphocytes but this was not closely related to the development of tubular injury. The reaction was maximum at one week and then decreased. Now, there was greater diversity of cells including macrophages, plasma cells and eosinophils, while many lymphoid cells became necrotic. It is concluded that most of the renal parenchymal injury is due to chemical mediators liberated from the infiltrating cells rather than to ischaemia or direct cytoplasmic interaction between leucocytes and tubular epithelium.
Local renal graft-versus-host reaction: sequential ultrastructural study. A sequential study has been made of the ultrastructure of local renal graft-versus-host reactions produced in cyclophosphamide-pretreated rats by injection of either allogeneic or xenogeneic (mouse) spleen cells beneath the renal capsule. Early in the reaction, immunoblasts were seen between the outer cortical tubules, and there was associated interstitial oedema and tubular degeneration. In places, several small lymphocytes were observed clustered around and in close cytoplasmic contact with individual immunoblasts, perhaps representing interaction between donor and host cells. As the reaction proceeded, the number of lymphoid cells increased by immigration from peritubular vessels. Some tubules were invaded by lymphocytes but this was not closely related to the development of tubular injury. The reaction was maximum at one week and then decreased. Now, there was greater diversity of cells including macrophages, plasma cells and eosinophils, while many lymphoid cells became necrotic. It is concluded that most of the renal parenchymal injury is due to chemical mediators liberated from the infiltrating cells rather than to ischaemia or direct cytoplasmic interaction between leucocytes and tubular epithelium.