Author/Authors :
Drake، نويسنده , , Charles G. and Doody، نويسنده , , Amy D.H. and Mihalyo، نويسنده , , Marianne A. and Huang، نويسنده , , Ching-Tai and Kelleher، نويسنده , , Erin and Ravi، نويسنده , , Sowmya and Hipkiss، نويسنده , , Edward L. and Flies، نويسنده , , Dallas B. and Kennedy، نويسنده , , Eugene P. and Long، نويسنده , , Meixiao and McGary، نويسنده , , Patrick W. and Coryell، نويسنده , , Lee and Nelson، نويسنده , , William G. and Pardoll، نويسنده , , Drew M. and Adler، نويسنده , , Adam J.، نويسنده ,
Abstract :
Summary
erstand the T cell response to prostate cancer, we created transgenic mice that express a model antigen in a prostate-restricted pattern and crossed these animals to TRAMP mice that develop spontaneous prostate cancer. Adoptive transfer of prostate-specific CD4 T cells shows that, in the absence of prostate cancer, the prostate gland is mostly ignored. Tumorigenesis allows T cell recognition of the prostate gland—but this recognition is tolerogenic, resulting in abortive proliferation and ultimately in hyporesponsiveness at the systemic level. Androgen ablation (the most common treatment for metastatic prostate cancer) was able to mitigate this tolerance—allowing prostate-specific T cells to expand and develop effector function after vaccination. These results suggest that immunotherapy for prostate cancer may be most efficacious when administered after androgen ablation.
