The Function and Role of the Th17/Treg Cell Balance in Inflammatory Bowel Disease

Abstract

Inflammatory bowel disease (IBD) is a chronic, inflammatory, and autoimmune disorder. The pathogenesis of IBD is not yet clear. Studies have shown that the imbalance between T helper 17 (Th17) and regulatory T (Treg) cells, which differentiate from CD4+ T cells, contributes to IBD. Th17 cells promote tissue inflammation, and Treg cells suppress autoimmunity in IBD. Therefore, Th17/Treg cell balance is crucial. Some regulatory factors affecting the production and maintenance of these cells are also important for the proper regulation of the Th17/Treg balance; these factors include T cell receptor (TCR) signaling, costimulatory signals, cytokine signaling, bile acid metabolites, and the intestinal microbiota. This article focuses on our understanding of the function and role of the balance between Th17/Treg cells in IBD and these regulatory factors and their clinical significance in IBD.

Stigmasterol Restores the Balance of Treg/Th17 Cells by Activating the Butyrate-PPARγ Axis in Colitis

“…Treg cells and Th17 cells perform specialized functions through distinct transduction pathways and restrict each other in terms of differentiation and function (4). Tregs have immunosuppressive properties that can also be present in the intestinal mucosa.…”

Emerging Perspectives of RNA N6-methyladenosine (m6A) Modification on Immunity and Autoimmune Diseases

“…Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation. Although the etiology of IBD is ill-defined, the dysregulation of proinflammatory Th17 cells and anti-inflammatory Treg cells contributes to the pathogenesis of IBD ( 78 , 79 ). Using CD4-Cre +/ Tg Mettl14 FL / FL conditional knockout mice, Thomas X et al firstly demonstrated that METTL14 deficiency in T cells causes the development of spontaneous colitis by dramatically increasing the release of Th17 cell-related proinflammatory cytokines ( 80 ).…”

Role of MicroRNA in Inflammatory Bowel Disease: Clinical Evidence and the Development of Preclinical Animal Models

“…Along with its role in innate immunity, it also plays a role in adaptive immunity by contributing to the differentiation of CD4+ T cells into various subsets of helper T cells (Th1, Th2, Th17) and Treg cells [ 170 ]. Th17 and Treg cells maintain a balance to ensure homeostasis, and dysregulation increases IBD susceptibility [ 171 ]. Singh et al found that 8–12-week-old miR-155 KO mice have lower levels of Th17 cells in the mesenteric lymph nodes in response to chronic DSS-induced colitis (1% DSS administered for seven days followed by seven days of water, treatment regime repeated for three cycles) along with reduced pro-inflammatory cytokines [ 116 ].…”