1. Figure 1 Overview of the immunopathogenesis of ulcerative colitis
and mechanisms of action of drugs with established efficacy in ASUC
Figure 1 | Overview of the immunopathogenesis of ulcerative colitis and mechanisms of action of drugs with established efficacy in ASUC. Glucocorticoids act in a number of ways (numbers in red stars): block the migration from neutrophils to the inflamed tissue (1); promote eosinophil apoptosis (2); diminish production of monocyte-derived or macrophage-derived inflammatory cytokines (3); inhibit macrophage phagocytic, antigen-presenting and microbicidal function (4); decrease the number of both circulating and organ-resident dendritic cells (5); induce apoptosis of immature T-cell subsets (6); inhibit the acute production of T helper (TH) 1- and, to a lesser extent, TH2-derived cytokines by activated T cells (7)11. Ciclosporin (number in orange star) inhibits the activation and proliferation of T cells and, to a lesser extent, B cells by blocking the transcription of their growth factor IL-2 (1)12. Infliximab acts in a number of ways (numbers in yellow stars): induces apoptosis of activated T cells (1); blocks TH1 effector functions (2); induces regulatory T (Treg)-cell activation and expansion, and enhances their suppressive function (3); reduces apoptosis of intestinal epithelial cells (4); promotes polarization of macrophages towards an anti-inflammatory phenotype (5); reduces the expression of endothelial adhesion molecules and blocks angiogenesis (6)13. ASUC, acute severe ulcerative colitis. IEL, intraepithelial lymphocyte. Figure modified with permission from an internal document by AbbVie.
Figure modified with permission from an internal document by AbbVie
Hindryckx, P. et al. (2016) Acute severe ulcerative colitis: from pathophysiology to clinical management
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro