| Summary: | 碩士 === 國立臺灣大學 === 生化科學研究所 === 97 === In this report, we have established a spontaneous tolerance model in which rats could develop spontaneous tolerance without any immunosuppressive treatments after orthotopic liver transplantion between DA (RT-1a) and PVG (RT-1c) rats. Functional proteomics analysis was introduced to investigate the differently expressed proteins involved in allograft liver transplantation. Among these different-expressed proteins, both haptoglobin and kininogen were reported to inhibit the proliferation of lymphocytes, suggesting a possible role of these two proteins in down-regulate cell-mediated graft rejection. Bioinformatics analysis of the statistically significant networks based on these differently expressed proteins indicated that the IL-6 signaling pathway might be involved in this model. IL-6 is a hepatoprotective cytokine that promotes liver regeneration, reduces liver injury and up-regulates the immune- suppressive proteins such as haptoglobin. Interestingly in this model, the highest expression of IL-6 occurred at the most severe stage of allograft rejection; thus we hypothesize that IL-6 might be the key contributor to spontaneous tolerance. Furthermore, it has been previously shown that IL-6 can also up-regulate the fucosylation regulatory genes, which supports our observation of an increase of fucosylation levels in serum protein; yet the related functions of fucosylation in this model remained unclear. These observations suggest that IL-6 plays a protective role in the spontaneous tolerance DA/PVG OLT model.
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