CD8(-REJECTION OR THE INDUCTION OF APOPTOSIS IN AN EXPERIMENTAL-MODELOF SMALL-INTESTINAL TRANSPLANTATION() CELLS ARE NOT NECESSARY FOR ALLOGRAFT)

Allospecific CTL can function as cellular effecters of solid organ gra ft rejection; hoc-ever, the specific mechanisms of cell damage remain undetermined. In this study we examined the role of CD8(+) T cells in apoptosis and rejection of small intestinal allografts, ACI rat intest inal grafts transplanted into Lewis rat recipients showed apoptosis of epithelial crypt cells on day 3 posttransplant as determined by termi nal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate ni ck end labeling staining, By day 7 numerous apoptotic crypt cells were detected in allografts, but were rarely observed in FK506-treated all ograft recipients, isografts, or native intestine of allograft recipie nts, To further investigate the mechanism of rejection, recipient rats were depleted of CD8(+) cells by treatment with OX-8 mAbs the day bef ore and the day after transplantation of rat small intestinal allograf ts, Depletion of CD8(+) cells from allograft recipients did not alter the tempo or the histologic features of rejection compared with those in the control (IgG-treated) group. Moreover, there was no difference in the number of apoptotic crypt epithelial cells in the grafts of con trol and CD8-depleted rats, Reverse transcriptase-PCR analyses determi ned there were similar levels of transcripts for Fas, Fas Ligand, perf orin, and granzyme B in control and CD8-depleted allograft recipients, By Western blot it was determined that the levels of Fas Ligand prote in were increased in the CD8-depleted group compared with those in con trol and FK506-treated allograft recipients, These data suggest that C DS cells are not required for tissue injury or apoptotic cell death in small intestine allograft rejection.