Experimental gene therapy mediated by fractalkine (FK) for murine liver cancer / 中华肝脏病杂志

<p><b>OBJECTIVES</b>Chemokines play an important role in the infiltration of immune cells into tumor tissues. Anti-tumor immune response has been elicited in many tumor models by chemokine gene transfection. The aim of this study was to evaluate the possibility of inducing anti-hepatocellular carcinoma active immune response by transfection of mouse hepatocellular carcinoma cells MM45T.Li with chemokine FK gene.</p><p><b>METHODS</b>Mouse FK gene was transduced into mouse hepatocellular carcinoma cells MM45T.Li using of liposome.G418-resistant clones were selected and the FK mRNA expression was detected by RT-PCR. In vivo experiments were performed to observe the tumorigenicity of wild type MM45T.Li and FK gene modified tumor cells. The immune cell infiltration in tumor tissues was detected histopathologically. The level of CD4+ and CD8+ T cells in peripheral blood were detected by FACS.</p><p><b>RESULTS</b>RT-PCR detection showed that FK was expressed in FK gene transfected G418-resistant clones (MM45T.Li-FK), but not in the wild type MM45T.Li. In vivo experiments the tumorigenicity of MM45T.Li-FK had decreased compared to the wild type MM45T.Li. In the tumor tissues from MM45T.Li-FK, many infiltrated immune cells were found, but few immune cells infiltrated into the tumor tissues from the controls. The level of CD4+ and CD8+ T cells had obviously increased in MM45T.Li-FK compared to the controls (P < 0.01).</p><p><b>CONCLUSION</b>Transfection with chemokine FK gene can induce anti-hepatocellular carcinoma active immune response.</p>

Expression of fractalkine and its receptor in acute cardiac allografts rejection / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the expression of fractalkine (FKN) and its receptor CX3CR1 in cardiac allografts and the effect of Cyclosporin A (CsA).</p><p><b>METHODS</b>Three groups of rats underwent heterotopic cardiac transplantation, 45 cases in each group and 5 cases in control group: SD to SD regarded as isograft group (group A), Wistar to SD divided into CsA untreated allograft group (group B) and CsA treated allograft group (group C), normal SD rats as control group. The FKN mRNA expression was detected by one-step RT-PCR method and the expression of FKN and CX3CR1 protein was detected by standard ABC immunohistochemical technique.</p><p><b>RESULTS</b>The expression of FKN mRNA and protein was weak in both isografts and normal heart specimens. The changes of FKN mRNA expression were correlated with the process of acute allograft rejection. The peak of FKN mRNA expression (0.8 +/- 0.26) appeared on the seventh day after transplantation, which could be down-regulated by CsA significantly (t = 2.390, P < 0.05). FKN protein was located in endothelia cells and its receptor CX3CR1 was located in infiltrating mononuclear cells in allografts.</p><p><b>CONCLUSIONS</b>Upregulation of FKN and its receptor was significantly correlated with the trafficking of mononuclear cells which play an important role in acute allograft rejection. It may be one of the important mechanisms of CsA to intervene the acute rejection by inhibiting the activation of the FKN-CX3CR1 pathway.</p>