The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses

Donor-specific blood transfusion (DSBT) given 1-2 weeks prior to transplantation prolongs the survival of fully allogeneic ACI (RT1") renal allografts in PVG (RT1^C) recipients from 6-8 days to >100 days. We have previously demonstrated that ACI kidneys transplanted to autologous blood transfusion (ABT)- or DSBT-pre-treated PVG recipients stimulated an increase in CD8⁺(OX8⁺) cells in the peripheral blood by 6 days after transplantation. To determine whether this increase represents a general expansion of the entire CD8⁺ population or only a subpopulation of CD8⁺ cells, subset analysis was performed on peripheral blood lymphocytes depleted of cells reactive with monoclonal antibodies against rat a/9 T cell receptor (TCR), CD8, or NK cells (R7.3, 0X8, or 3.2.3, respectively). Phenotypic studies of PBL depleted of CD8⁺ cells demonstrated that all 3.2.3⁺ NK cells coexpressed CD8; depletion of 3.2.3* PBL revealed a secondsubpopulation of CD8⁺3.2.3~ cells comprised predominantly of a/8TCR⁺ T cells. In naive PVG rats the prevelence of these two CD8 subpopulations was approximately equal. Both ABT- and DSBT-pretreated renal allograft recipients demonstrated a significant and equivalent expansion of the CD8⁺ cell subpopulation that coexpresses the 3.2.3 NK marker. In contrast, the second subpopulation of CD8+3.2.3^- cells did not change significantly after allografting. There were also no differences between DSBT and ABT pretreated rats in activity of PBL against the NK targets YAC-1 and Doxie at 6 days after renal transplantation, though the level of activity was modestly increased compared with naive controls. These findings indicate that renal transplantation in the rat is associated with a significant increase in PBL with the NK phenotype (CD8⁺3.2.3⁺) and a modest increase of NK activity, but that DSBT enhancement does not affect this NK cell response.