Immunologic monitoring of the beneficial effect of one HLA-DR-shared bloodtransfusion in heart transplant patients

Background: Pre-transplant blood transfusion (BT) results in better graft s urvival in organ transplant recipients, especially when BT donor and allogr aft recipient share an HLA-DR antigen. Although the immunologic mechanisms involved are still poorly understood, we wanted to know whether down regula tion of donor-reactive T cells play a role. Methods: In a retrospective study, we analyzed the clinical effects of BT f or 45 heart transplant (HTx) patients who had each received 1 BT that share d an HLA-DR-antigen with the recipient, and 55 who had a DR-mismatched BT b efore heart transplantation. From 30 patients, 15 with DR-shared BT and 15 with DR-mismatched BT, peripheral blood lymphocytes (PBL) were available. F rom each patient, we analyzed PBL samples taken at the day of transplantati on (pre-transplant), and 1 to 2 months, 5 to 7 months, 9 to 14 months, 2 ye ars, and 6 to 7 years after transplantation. Cytotoxic T-lymphocyte precurs ors (CTLp) and helper T-lymphocyte precursors (HTLp) were measured in a com bined limiting dilution assay. Results: Analysis of survival during the first 10 years revealed a signific antly (p = 0.016) better survival rate in the group of patients who had rec eived HLA-DR-shared BT compared with the group who had received HLA-DR-mism atched BT. Patients of the DR-shared group experienced significantly (p = 0 .042) less acute rejections compared with the patients who received DR-mism atched BT. We found no differences in the development of graft vascular dis ease. Frequencies of CTLp specific for the organ donor did not change with time after transplantation in the individual patients, nor did we detect an y differences between the two BT groups. We found the same for organ donor- specific HTLp frequencies. Conclusions: These data suggest again that transfusion effect depends on HL A-DR compatibility between the heart transplant recipient and the pre-trans plant BT donor. The mechanism that caused better survival rate was not down regulation of the donor-reactive T-cell frequency.