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.

DeNardo and Coussens Breast Cancer Research 2007 9:212   doi:10.1186/bcr1746
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