Thus, MSC treatment reduced the clinical and histopathological severity in experimental animal models of colitis by downregulating the Th1 and Th17-driven inflammatory response (i.e. reduction of pro-inflammatory cytokines such as tumor necrosis factor (TNF), interferon gamma (IFNγ), interleukin (IL)-6, IL-12 or IL-17), increasing the levels of anti-inflammatory cytokines such as IL-10, and promoting the generation of immune cells with immunomodulatory properties such as FoxP3 regulatory T cells, regulatory B cells, and M2 macrophages [13–18]. Here, TNF is linked to colitis.