Although small differences in T cell proliferation activity and CTL cytotoxicity were observed between hTERTC27 treated mice and control group mice, induced by rAAV-/rAdvhTERTC27 observed in our study. A minor increase of CTL cytotoxicity in spleen lymphocytes might be a result of increased levels of Th1 cytokine in blood. A considerable increase in the levels of IL-2, IFN-c and GM-CSF was observed in the plasma of mice treated with rAAV-/rAdv-hTERTC27 compared with the control mice. All these cytokines function as an immune adjuvant and are known to contribute to the development and activity of tumor specific CTL. However, further investigation is required to determine whether cytokines such as IL-2 and IFN-c could increase the population of cytokine-inducedkiller cells in vivo and contribute to the antitumor effects of hTERTC27. Unlike our previous study in which ectopic expression of rAAV-hTERTC27 in nude mice significantly upregulated the IL-17 mRNA level in xenografted tumor tissue, administration of rAAV-/rAdv-hTERTC27 viral cocktail in C57BL/6 mice showed a little increase of IL-17 cytokine level in blood in this study. The discrepancy may come from the different mouse models and delivery systems used between these two studies. Nonetheless, the slight change in IL-17 level is FG-4592 consistent with the mild increase in activated T cells because it is known that IL-17 expression is restricted to activated T-cells. It is worth noting that NK cells are known to play a major role in cytokine-mediated inhibition of B16 melanoma development and that IL-2 can induce the proliferation and activity of NK cells. Moreover, activated NK cells can secrete several cytokines, including IFN-c and GM-CSF and increase IL-2 mRNA expression. In addition, IFN-c itself also activates NK cells. Because of the complex relationship between NK cells and these cytokines, the initial effect following hTERTC27 administration remains elusive and requires further investigation. Elevated levels accurately reflect the presence of neuropathological conditions including traumatic head injuries, psychiatric disorders, cerebrovascular insults and neurodegenerative diseases, while normal levels reliably exclude major CNS pathology. Its potential clinical use in the therapeutic decision making process is substantiated by a vast body of literature validating variations in serum 100B levels with standard modalities for prognosticating the extent of CNS damage: alterations in neuroimaging, cerebrospinal pressure, and other brain molecular markers. Thus, the major advantage of using S100B is that elevations in serum can be easily measured, providing a sensitive measure to help rule out major CNS dysfunction. An important application of serum S100B testing is the selection of patients with minor head injury who do not need further neuroradiological evaluation, as studies comparing CT scans and S100B levels have demonstrated S100B values below 0.1 ng/mL are associated with low risk of obvious neuroradiological changes or significant clinical sequelae.