抄録
Non-human primate is an invaluable model for biomedical studies on immunology because of highly close similarity in genomic and other biological events with those of human. Up to date little information about immune response in non-human primate has been accumulated. In this study we examined biomedical characteristic of gene expression profile of primate cytokines (IL-4, IL-12 and IFN-γ ) and their receptors (IL4Rα , IFN-γ R1 and IFN-γ R2) by real time RT-PCR.
Total RNA from peripheral blood mononuclear cells (PBMC) of human, ape (chimpanzee) and monkeys (cynomolgus, rhesus and Japanese macaques, green monkey and baboon) was purified with QIAGEN RNeasy micro kits. Thus obtained RNA was subjected to analysis of gene expression profile by real time RT-PCR. Briefly, after reverse transcription of each RNA with oligo-dT primer, following real time PCR was preformed by use of resulting cDNA, specific primers, TAKARA pre-mix, and SYBR Green I with ABI 7700 Sequence Detection System. Relative gene expression was quantified from that of a house keeping gene, GAPDH, using a calibration curve of GAPDH.
In human and chimpanzee, the gene expression levels of a Th2 cytokine, IL-4, were significantly higher than those in monkeys, whereas the gene expression levels of a Th1 cytokine, IL-12, were apparently higher in monkey. Thus, these gene expression profiles were anti-parallel in primates. The gene expression levels of IFN-γ and IL4Rα were almost same among human, chimpanzee and monkeys. Interestingly, the gene expression levels of IFN-γ R1 and IFN-γ R2 in cynomolgus macaque were the highest among primates examined here. The expression levels of IFN-γ R1 and IFN-γ R2 genes in cynomolgus macaque were also markedly higher than those of close-related macaques, rhesus and Japanese macaques.
These results indicate that human and chimpanzee have similar characteristics in immunological events, but distinguishable from monkeys. Among macaques, cynomolgus macaque appears to have a unique immunological characteristic in IFN-γ /IFN-γ R pathway associating with Th1 response, which could affect susceptibilities to Th1-mediated pathogenic event such as tuberculosis.