BACKGROUND: Immunopotentiating agents are the best options in cancer therapeutics because they can specifically destroy tumor cells via immunocytes, which are mostly apoptotic in nature. Previously, immunotherapy with T11TS / SLFA-3 in a ethyl-nitrosourea (ENU)-induced animal model (Druckrey rats) of neural neoplasm showed a significant tumor mass destruction by augmenting the cellular immune status. MATERIALS AND METHODS: The modulations of the peripheral as well as neural immune systems after T11TS administration were monitored by assessing the CD4+ and CD8+ lymphocytes, along with the cytotoxic activity of splenic and brain infiltrating lymphocytes (BIL). The rate of apoptosis of the tumor cells, microglial cells (Mg) and BIL were measured by flow cytometry-based propidium iodide analysis and TUNEL assay. RESULTS: Cell cycle phase distribution analysis by propidium iodide -FACS and TUNEL assay revealed that T11TS administration gradually increased the number of apoptotic brain tumor cells and, at the same time, decreased the number of dividing cells. Up-regulation of the CD4+ and CD8+ lymphocytes were observed after T11TS administration in ENU - induced immunosuppressed animals. A gradual increment of cytotoxicity of splenic and BIL was also demonstrated after successive administration of T11TS. CONCLUSION: These data strongly support the specific apoptosis-inducing role of T11TS in experimental brain tumor cells. Apoptosis of BIL and Mg, that occurred to a much lower level, can be explained in terms of changes in the neural immune system before and after T11TS application.
BACKGROUND: Immunopotentiating agents are the best options in cancer therapeutics because they can specifically destroy tumor cells via immunocytes, which are mostly apoptotic in nature. Previously, immunotherapy with T11TS / SLFA-3 in a ethyl-nitrosourea (ENU)-induced animal model (Druckrey rats) of neural neoplasm showed a significant tumor mass destruction by augmenting the cellular immune status. MATERIALS AND METHODS: The modulations of the peripheral as well as neural immune systems after T11TS administration were monitored by assessing the CD4+ and CD8+ lymphocytes, along with the cytotoxic activity of splenic and brain infiltrating lymphocytes (BIL). The rate of apoptosis of the tumor cells, microglial cells (Mg) and BIL were measured by flow cytometry-based propidium iodide analysis and TUNEL assay. RESULTS: Cell cycle phase distribution analysis by propidium iodide -FACS and TUNEL assay revealed that T11TS administration gradually increased the number of apoptotic brain tumor cells and, at the same time, decreased the number of dividing cells. Up-regulation of the CD4+ and CD8+ lymphocytes were observed after T11TS administration in ENU - induced immunosuppressed animals. A gradual increment of cytotoxicity of splenic and BIL was also demonstrated after successive administration of T11TS. CONCLUSION: These data strongly support the specific apoptosis-inducing role of T11TS in experimental brain tumor cells. Apoptosis of BIL and Mg, that occurred to a much lower level, can be explained in terms of changes in the neural immune system before and after T11TS application.