In patients with cancer, alterations also occur in systemic antitumor immunity [56, 131, 190, 192]. In a tumor-bearing host, dissemination of antigens released from the growing (shed or secreted antigens) or dying (apoptotic/necrotic debris) tumor cells assures their access to APC and allows for the cross-priming of immune effector cells in lymphoid tissues draining the site of the tumor. It is likely that the composition, number and the state of activation/differentiation of the immune infiltrate at the local site will vary over time, depending on the evolving (constitutive or therapy induced) systemic immune response of the host to TAA and the ability of these cells to be recruited into and survive/function within the tumor microenvironment. Circulating T cells obtained from patients with cancer are either biased in their cytokine profile or otherwise functionally compromised [17, 131, 171]. Furthermore, dysfunctions in circulating lymphocytes was linked to the extent of dysfunction seen in paired TIL  and to the disease stage and/or activity [24, 131]. Thus, patients with advanced stage carcinomas had more lymphocyte dysfunction (low Z expression, low proliferative index, greater NFkB dysfunction) than patients with early or inactive disease [24, 131]. The presence of such systemic alterations may explain, in part, why vaccines and other immunotherapies yield objective clinical responses in only a small minority (at best 20%) of patients with cancer.
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