T cells mount main vaccine defense against HER-2 tumors
T cells are the main effector cells in DNA vaccine induced immunity against HER-2/neu (HER-2) expressing tumors. Thus, anti-HER-2 antibodies are not needed to prompt tumor rejection, researchers report in the March 20th issue of the International Journal of Cancer.
Dr. Rolf Kiessling of the Karolinska Hospital, Stockholm, and colleagues note that HER-2 is an oncogene implicated in a variety of cancers.Anti-HER-2 antibodies have shown some success in treatment of breast tumors. Nevertheless, the researchers point out that the contribution of B cells and antibodies relative to that of T cells in tumor rejection in HER-2 vaccination models “remains unclear.”To investigate further, the team studied mice immunized using plasmid HER-2 and GM-CSF. Among findings were that protection was associated with the production of anti-HER-2 IgG antibodies in B cell competent mice.However, when the same procedure was used in B cell-deficient mice, these animals “rejected HER-2 expressing tumors as efficiently as control littermates.” Tumor protection was afforded in the absence of antibodies.”These results,” the researchers conclude, “therefore argue that tumor-reactive antibodies, induced by vaccination or by a significant tumor burden, may not be needed for tumor rejection and thus are dispensable.”GM-CSF co-administration was needed to afford “strong protection” in both groups of mice, the investigators add.They conclude that further efforts should be made “toward developing T cell dependent tumor vaccination strategies based on HER-2.”(Source: Int J Cancer 2004;109:259-264: Reuters Health: Oncolink: April 2004)