Figure 4.

Model depicting the consequences of acute inflammation versus chronic inflammation. During acute antitumor inflammatory responses (left panel), Th1-polarized T cells secrete antitumor cytokines (IL-2 and INFγ, for example), which in combination with antitumor-directed B-cell-derived factors (such as immunoglobulins (Igs)) activate tumor inhibitory responses in recruited innate immune cells and cytotoxic T lymophocytes (CTLs) that together favor tumor rejection. In contrast, chronic activation of immune response (right panel) without resolution (of damage) often results in accumulation of regulatory T (Treg) cells, Th2 cells, and activated B cells, which in turn secrete progrowth factors (IL-4, IL-6, IL-10, IL-13, transforming growth factor beta (TGFβ) and immunoglobulins, for example) that enhance protumor responses in innate immune cells and inactivate CTL cytotoxicity, thus favoring tumor promotion.