The increase in the steady-state level of major histocompatibility complexmRNA in the host peripheral T lymphocytes due to ischaemia-reperfusion injury

In our previous study, using a swine model of single lung transplantation, a relationship between the level of major histocompatibility complex (MHC I I) expression on host T lymphocytes and the extent of the eu vivo preservat ion time was observed. Furthermore, a model of ischaemia by simple cross-cl amping proved MHC II up-regulation to be independent of tissue incompatibil ity. The mechanism through which ischaemia-reperfusion injury (IRI) induces MHC up-regulation in host peripheral T cells has not been reported. The ob jective of this study was to determine whether IRI induces MHC II up-regula tion in T cells by altering the intracellular steady-state level of MHC II mRNA. Group A (seven donors, seven recipients) was an allotransplantation model o f 15 h of cold storage (4 degrees C) while in group B (n = 6) animals under went 2 h of warm ischaemia. Group C (n = 6) underwent sham operation. For q uantification of mRNA extracted from peripheral T lymphocytes isolated befo re and after surgery, semi-quantitative reverse transcription polymerase ch ain reaction (RT-PCR) was used to determine the time at which mRNA levels r eached its peak. The mRNA at pre-reperfusion and the time, at which mRNA pe aked, was used for competitive RT-PCR. The results of RT-PCR analyses demonstrated that IRI induced an increase in the steady-state level of MHC II mRNA (p < 0.02) within 2 h post-reperfusi on, irrespective of type of ischaemia and tissue incompatibility. In conclu sion, this study suggested that IRI up-regulates the MHC II expression in p eripheral T cells by altering the intracellular steady-state level of MHC I I-DR-beta.