In deceased donors, Ischemia/Reperfusion Injury (IRI) is an important cause of allograft
dysfunction. Prolonged cold and warm ischemia time leads to a high risk of early post-transplant
complications, including acute and chronic rejection. Ischemia not only up-regulates inflammatory
cytokines and chemokines, but also enhances the expression of MHC-class II and adhesion molecules
on epithelial and dendritic cells. Moreover, the Danger Associated Molecular Patterns (DAMPs) released
from stressed or dying cells, not only cause or amplify tissue inflammation and trigger tissue
repair in response to IRI, but also act as adjuvants that enhance DC maturation and potentiate the
adaptive immune response. In this review, we will also discuss about whether donor or recipient DCs
are more important in the process of ischemia enhanced acute rejection.
Keywords: Dendritic cells, Kidney transplantation, Allograft rejection, Ischemia/reperfusion injury, APC, CTLs.
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