In accordance with findings showing that therapeutic antibodies blocking TNF-α enhanced IL-10 production by all effector T cell subsets in vitro [103,104], targeting tumor necrosis factor receptor 1 assembly was shown to suppress Th1 and Th17 effector phenotypes by increasing the frequency of IL-10-producing populations and the levels of IL-10 in Th1 and Th17 cells in a T cell-specific, Blimp-1-deficiency-mediated colitis model [105]. This evidence concerns the gene IL10 and colitis.