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Cutting edge: perforin down-regulates CD4 and CD8 T cell-mediated immune responses to a transplanted organ.
Perforin mediates target cell apoptosis by CTLs and NK cells. Although perforin expression correlates strongly with acute allograft rejection, perforin-deficient mice reject allografts with the same kinetics as wild-type recipients. In this study, we tested the hypothesis that while perforin is dispensable for acute rejection, it is essential for down-regulating the alloimmune response by inducing the apoptosis of host immune cells. Using a skin transplantation model, we found that perforin-deficient mice are resistant to the induction of allograft acceptance by agents that block T cell costimulation. Failure to induce allograft acceptance in these mice was observed irrespective of whether the alloimmune response was CD4 or CD8 T cell-mediated and could be attributed to defective apoptosis of activated CD4 and CD8 T cells. In contrast, perforin did not influence T cell proliferation. Therefore, perforin is an essential immunoregulatory molecule that may be required for the induction of transplantation tolerance.[1]References
- Cutting edge: perforin down-regulates CD4 and CD8 T cell-mediated immune responses to a transplanted organ. Bose, A., Inoue, Y., Kokko, K.E., Lakkis, F.G. J. Immunol. (2003) [Pubmed]
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