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+ Dendritic Cells Prolong the Survival of Vascularized Heart Allografts1
,
*
Thomas E. Starzl Transplantation Institute and Departments of
Surgery and
Molecular Genetics and Biochemistry, University of Pittsburgh Medical Center, Pittsburgh, PA 15213
CD8
+ and CD8- dendritic cells (DCs)
arise from committed bone marrow progenitors and can induce or regulate
immune reactivity. Previously, the maturational status of
CD8- (myeloid) DCs has been shown to influence
allogeneic T cell responses and allograft survival. Although
CD8+ DCs have been implicated in central tolerance and
found to modulate peripheral T cell function, their influence on the
outcome of organ transplantation has not been examined. Consistent with
their equivalent high surface expression of MHC and costimulatory
molecules, sorted mature C57BL/10J (B10; H2b) DCs of either
subset primed naive, allogeneic C3H/HeJ (C3H; H2k)
recipients for Th1 responses. Paradoxically and in contrast to their
CD8- counterparts, mature CD8+ B10 DCs
given systemically 7 days before transplant markedly prolonged B10
heart graft survival in C3H recipients. This effect was associated with
specific impairment of ex vivo antidonor T cell proliferative
responses, which was not reversed by exogenous IL-2. Further analyses
of possible underlying mechanisms indicated that neither immune
deviation nor induction of regulatory cells was a significant
contributory factor. In contrast to the differential capacity of the
mature DC subsets to affect graft outcome, immature CD8+
and CD8- DCs administered under the same experimental
conditions significantly prolonged transplant survival. These
observations demonstrate for the first time the innate capacity of
CD8+ DCs to regulate alloimmune reactivity and
transplant survival, independent of their maturation status.
Mobilization of such a donor DC subset with capacity to modulate
antidonor immunity may have significant implications for the therapy of
allograft rejection.
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