Fig. 1Histology of colon tissue from IBD patients. (A) H&E of colon tissue from UC and CD patients (H&E, ×40). (B, C) Signal transducer and activator of transcription 3 (STAT3) and interleukin 17 (IL-17) expression in colon tissue from UC and CD patients (immunohistochemistry, ×200).
Fig. 2Pathogenic innate lymphoid cells (ILCs) and T cells in mucosal cells from IBD patients. ILCs have common properties with T effector cells. Lineage-specific transcription factors expressing ILCs or a subset of T cells produce the same cytokine. Natural cytotoxicity receptor (NCR)-expressing ILCs are classified differently from T cells. T-bet, T-box expressed in T cells; IFN, interferon; TNF, tumor necrosis factor; IL, interleukin; RORγt, retinoic acid receptor-related orphan receptor γt.
Fig. 3Present IBD therapeutic strategies that involve prevention of T cell and innate lymphoid cells (ILC) production or their inhibition. T cells and ILCs have a common therapeutic target. Compared with classical IBD therapeutic agents, new therapeutic strategies may involve T cells; ILCs such as interleukin (IL)-23 and IL-12-, tumor necrosis factor (TNF)-, and integrin-targeting agents; and signal transducer and activator of transcription (STAT) inhibitors. NF, nuclear factor; AP-1, activator protein 1; cAMP, cyclic adenosine 3′:5′-monophosphate.
Fig. 4Reciprocal balance for intestinal immune homeostasis and inflammation. The normal state is mediated by a reciprocal balance between immune cells (Treg and Breg vs. Th17 and ILC1) and cytokines that are secreted to maintain the conditions in the intestine. However, an imbalance in immune cells leads to the destruction of intestinal epithelial cells and the invasion of commensal microbiota. This situation leads to the uncontrolled release of cytokines, which is a key event in the pathogenesis of IBD. Treg, regulatory T; Breg, regulatory B; ILC, innate lymphoid cells; DC, dendritic cell; IL, interleukin; NKT, natural killer T; Th17, T helper 17.