FOXP3 and neoplasm: Lastly, recent studies have shown that endogenous IL-10 can potentially limit the pro-tumor and/or antitumor effects of Th17-mediated inflammation either indirectly by promoting the regulatory functions of both FoxP3+ and FoxP3− cells or directly by interacting with IL-10 receptors on Th17 cells in an IL-10 signaling-dependent manner (Chaudhry et al., 2011; Huber et al., 2011).