Upon pathogen infection, both proinflammatory and antiinflammatory cytokines are produced by activated myeloid cells. In addition to their direct effects on tumor cell growth, survival, and invasive properties, cytokines can govern the functions of Th1 cells, NK cells, Tregs, and Th17 cells, all of which infiltrate the tumor. Treg-mediated suppression of antitumor CTL responses and induction of inflammatory Th17 cell–mediated responses contribute to tumor progression. Paradoxically, IL-10 can mediate the antitumor effects of Tregs. IL-23, TGF-β, IL-6, and TNF-α promote the development of Th17 cells, which have a central role in coordinating chronic inflammatory responses. IL-23 can induce the release of IFN-γ and IL-12 from activated T cells, TNF-α and IL-12 from APCs, and IL-17 from Th17 cells. In certain cases, cytokines such as TNF-α and IL-6 might be produced by tumor cells and function in an autocrine and paracrine fashion.