[Recombinant eukaryotic expression plasmid of bcr-abl gene fragment induces specific immune response in mice].

To study the specific immune response induced by a recombinant eukearyotic expression plasmid encoding bcr-abl fusion gene fragment so as to explore new immunotherapy in mouse. Methods A recombinant eukaryotic vector pVbcr-abl expression cDNA fragment of bcr-abl fusion gene was constructed and used to immunize BALB/c mice. Serum level of bcr-abl specific antibody was detected by enzyme-linked immunosorbent assay ( ELISA). Twenty days later the immunized mice were subcutaneously inoculated SP2/0/bcr-abl cells. The survival time, tumor growth time and lymphocytic infiltration were observed. T cells infiltration into tumor tissue was analyzed by immunohistochemistry. Changes of T cell subset in the spleen of mice was analyzed by fluorescent-activated cell sorting (FACS) and the cytotoxicity T lymphocyte (CTL) activity in spleen by lactate dehydrogenase ( LDH)-release assay. Results The eukaryotic expression vector pVbcr-abl was constructed successfully, and highly expressed the cDNA fragment of bcr-abl fusion gene. The BALB/c mice immunized with the vector could generate the specific antibody and CTL, resulting in a specific immunoprotection. There were dramatic differences in the tumor-forming time, tumor ulcer appearring time and tumor-growing speed between the immunized and the control groups. The mice had longer survival time in the immunized group than in the control group. There were a large amount of CDS + T cells infiltration in tumor tissue of the immunized mice. The spleen cells from the immunized mice had higher CTL activity with a alteration of T cell subset, the CD4+ /CD8+ ratio being 1.54 ± 0. 29, higher than that of control group (1. 18 ±0. 30). Conclusion The recombinant eukaryotic expression plasmid pVbcr-abl can induce in vivo not only the generation of specific antibody, but also high level of specific CTL activity, resulting in killing the SP2/0/bcr-abl tumor cells directly and inhibiting the tumor growth.