Modulators of arginine metabolism do not impact on peripheral T-cell tolerance and disease progression in a model of spontaneous prostate cancer

摘要: Purpose: Chronic inflammation, recruitment of myeloid-derived cells, and perturbation the arginine metabolism have been all proposed as mechanisms favoring prostate carcinogenesis tumor immunoescape. Objective this study was to evaluate whether accumulation CD11b + Gr1 also defined suppressor occur in mice affected by transplantable or spontaneous cancer (PC). We investigated N(G) nitro-l-arginine methyl ester (l-NAME) sildenafil, both modulators metabolism, restrain growth restore tumor-specific immunity. Experimental Design: Wild-type C57BL/6 bearing TRAMP-C1 PC transgenic adenocarcinoma mouse (TRAMP) were treated with vehicle, l-NAME evaluated for cells blood, several organs, mass disease progression. Results: high , int − differently accumulated different organs especially two models. sildenafil impaired immunosuppressive function models restrained growth, but they neither break immune tolerance nor limit progression TRAMP mice. Conclusions: Collectively, our results emphasize substantial differences tumor-induced alteration myelopoiesis sensitivity between a model PC. They suggest that is dispensable associated T-cell tolerance. Clin Cancer Res; 17(5); 1012–23. ©2011 AACR .