1999; Eton, Legha et al. 2002; Kwak 2003; Kaufman, Wang et al. 2004; Coppin, Porzsolt et al. 2005). In a majority of these trials, induction of tumor specific cellular immune responses have been document ed. However, in only a minority has there been translation into clinical effectiveness (Walden 2007). There have been several hypotheses to explain this demonstrable lack of anticancer immune activity in solid tumors . These include ine ffective priming of tumor-specific T cells, lack of high-avidity of primed tumor-specific T cells, and physical or functional disabl ing of primed tumor-specific T cells by the primary host and or tumor-related mechanism. For example, in NS CLC a high proportion of the tumor-infiltrating lymphocytes ar e immunosuppressive T regulatory cells (CD4+ CD25+) that secrete tr ansforming growth factor- β (TGFβ) and express a high level of cytotoxic T lymphocyte (CTL) antigen-4 (Woo, Yeh et al. 2002). These cells have been shown to impede immune activation by facilitating T cell tolerance to tumor associated antigens ra ther than cross-priming CD8+ T cells, resulting in the inhibition of killer T cells that recognize the tumor without attacking it (Dohadwala, Luo et al. 2001; N euner, Schindel et al. 2002; Woo, Yeh et al. 2002). Elevated levels of immune inhibitors such as IL-10 and TGF β are found in the circulation in patients with advanced cancer, and animal models have shown immune suppression is mediat ed by these cytokines serving both as a barrier to antigen recognition and T-cell activation, as well as a defense against the body’s immune effector system (Rook, K ehrl et al. 1986; Tsunawaki, Sporn et al.