Abstract
Allograft rejection is a complex process, which requires interactions between different cell types and a variety of soluble factors, such as cytokines. In this review we discuss the role of cytokines in the induction and effector phases of the rejection process and in the induction and maintenance of allospecific graft tolerance. Furthermore, we discuss the feasibility of clinical graft function monitoring by measuring cytokines and the possibilities for intervention in the cytokine network in order to inhibit graft rejection and eventually obtain graft acceptance.
Highlights
Cytokines are proteins, which act as soluble mediators and regulators of immune responses
Anti-IFN-7 antibodies alone failed to prolong graft survival compared with untreated controls.,[1] in combination with cyclosporin A (CsA), antiIFN-y antibodies prolonged allograft survival in a synergistic way.,[2] This synergistic action with CsA, that permits lowering of the CsA dose, thereby decreasing its potential nephrotoxicity, is seen using anti-TNFmt antibodies.[8,69]
In an allogeneic graft model, the use of anti-IFN-7 or anti-IL-2 monoclonal antibody (mAb) has not been very effective in prolonging allograft survival, as we described earlier
Summary
AttOaSA rejection is a complex process, which requires interactions between different cell types and a variety of soluble factors, such as cytokines. In this review we discuss the role of cytokines in the induction and effector phases of the rejection process and in the induction and maintenance of allospecific graft tolerance. We discuss the feasibility of clinical graft function monitoring by measuring cytokines and the possibilities for intervention in the cytokine network in order to inhibit graft rejection and eventually obtain graft acceptance. Key word: Cytokines, Graft rejection, Monoclonal, antibody treatment, Thl-Th2 subsets, Tolerance
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