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We report the use of PDE5 inhibitors as modulators of the antitumor immune response. In several mouse tumor models, PDE5 inhibition reverses tumor-induced immunosuppressive mechanisms and enables a measurable antitumor immune response to be generated that substantially delays tumor progression. In particular, sildenafil, down-regulates arginase 1 and nitric oxide synthase–2 expression, thereby reducing the suppressive machinery of CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) recruited by growing tumors. By removing these tumor escape mechanisms, sildenafil enhances intratumoral T cell infiltration and activation, reduces tumor outgrowth, and improves the antitumor efficacy of adoptive T cell therapy. Sildenafil also restores in vitro T cell proliferation of peripheral blood mononuclear cells from multiple myeloma and head and neck cancer patients. In light of the recent data that enzymes mediating MDSC-dependent immunosuppression in mice are active also in humans, these findings demonstrate a potentially novel use of PDE5 inhibitors as adjuncts to tumor-specific immune therapy. levitra coupons order viagra canada online Figure 8. PDE5 inhibition restores proliferation of head and neck and myeloma lymphocytes. (A) Unfractionated or CD14-depleted PBMCs from MM patients were stimulated with anti-CD3/CD28 antibody–coated beads in the presence of NorNOHA, L-NMMA, both NorNOHA and L-NMMA, sildenafil, or no inhibitor. The CD3+ T cell expansion was measured 5 d later by flow cytometry. (B) Ficoll-purified PBMCs from healthy donors (n = 4), head and neck cancer patients (H &N; n = 7), or MM patients (n = 7) were stimulated as described in A in the presence or absence of sildenafil. CD4+ and CD8+ T cell expansion was measured by flow cytometry 5 d later. Data are reported as fold change. t test p-values are reported. Horizontal lines represent the median, the 10th and 90th percentile.