Donor-specific blood transfusion prolongs survival of fully allogeneic ACI (RTla) renal grafts in PVG (RT1C) recipients from 6-8 days to >100 days. To determine how DSBT alters effector cytotoxic cell responses, we tested freshly isolated peripheral blood lymphocytes, spleen cells, and graft infiltrating cells (GIC) from pairs of PVG recipients of ACI kidneys pretreated with DSBT or autologous blood transfusion (ABT) for cell-mediated lympholysis, antibody-dependent cellular cytotoxicity (ADCC), and natural killer activity at the day of transplantation (day 0) and days 3 and 6 posttransplantation. PBL and GIC from the same pairs of animals were examined for their phenotypic profile (CD4, CD8, 3.2.3 NK cell marker, IL-2 receptor). CML, ADCC, and NK activity were higher in PBL than splenocytes or GIC of both ABT and DSBT groups at all time points examined. CML activity of PBL at day 3 was significantly higher in DSBT vs. ABT recipients (P+ cells and increases in CD8+ and 3.2.3+(NK) cells. The percentage of IL-2R+ cells remained low (+ (and to a lesser extent CD4+) GIC in ABT- but not DSBT-treated recipients, while CD8+cells were significantly increased in both groups. These findings indicate that DSBT enhancement of rat renal allografts does not result in the functional deletion or depletion of CML, ADCC, or NK cytotoxic effector cells in PBL, spleen, or allograft at early times after transplantation (day 3), and only a modest reduction in CML activity of splenocytes at day 6. Furthermore, CD8+and 3.2.3+cells in PBL and the graft do not appear to be affected by DSBT enhancement, whereas the significant increase in IL-2R+(and CD4+) infiltrating cells seen in rejecting ABT controls is not observed in DSBT animals. These results suggest that DSBT enhancement in the rat is more likely to be the result of diminished alloimmune responsiveness involving noncytolytic lymphocyte functions, such as alloantibody production and delayed-type hypersensitivity.
|Original language||English (US)|
|Number of pages||9|
|State||Published - 1991|
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