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Evidence that host immunity plays a critical role in limiting tumor outgrowth in the early stages of tumorigenesis supports the notion of immune surveillance (1, 2). However, to effectively function, endogenous or adoptively transferred tumor-specific T cells must be present in reasonable numbers, maintain their tumor specificity and an activated phenotype, traffic to the tumor site, and kill their targets in situ. Unfortunately, priming tumor-specific T cells and sustaining an immune response that imparts a measurable clinical benefit is limited by the ability of tumors to modify their microenvironment (3). These immunosuppressive mechanisms are also present in transplantable mouse tumors in which stable cell lines are generated after multiple in vivo passages that ultimately select for clones able to avoid immune recognition. As such, these models represent useful tools to identify the cellular and molecular tumor-induced immunosuppressive pathways, as well as discover pharmacological targets and screen immunomodulatory drugs with measurable antitumor activity.
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