Plasticity of Th17 and Tregs and its clinical importance as therapeutic target in inflammatory bowel disease

Abstract

The gut immune system is very complex and a single layer of the epithelial barrier along the gastrointestinal tract prevents the evasion of various extracellular commensal and pathogenic microorganisms in the gut mucosa. The inflammatory bowel disease (IBD) consists of ulcerative colitis (UC) and Crohn’s disease (CD). The cause of IBD is thought to be associated with genetic, epigenetic, environmental factors, dietary habits and gut microbiota. Immunologically, the effector CD4+ T cells such as Th1, Th17, and regulatory CD+ T cells play an important role in the pathogenesis of IBD. During gut inflammation and autoimmunity, these cells show phenotypic and functional plasticity, and differentiate into other lineages as well as have mixed-lineage phenotypes such as Th1-Th17, Th1-Treg, and Th17-Treg. The present review discusses the intrinsic and extrinsic factors that affect the cellular and molecular plasticity of Th17 and Treg, their clinical importance, and how plasticity and reprogramming of these cells can be targeted to control the IBD.