Traditional Chinese Medicine Regulates Th17/Treg Balance in Treating Inflammatory Bowel Disease

Figure 1

Mechanism of action of the monomers and compound formulations of traditional Chinese medicine. Under normal conditions, the intestine does not produce IL-6 due to the lack of pathogen stimulation from antigen-presenting cells, and naïve CD4+ T cells mainly differentiate into Treg cells under TGF-β to prevent the occurrence of autoimmune disease. When pathogens invade, antigen-presenting cells can secrete IL-6, and IL-6 acts together with TGF-β to induce the differentiation of naïve CD4+ T cells to Th17 cells and to inhibit the induction effect of TGF-β on Treg, with an enhanced immune response, contributing to the elimination of pathogens. When the inflammatory effect of Th17 cells exceeds the tolerance effect of Treg cells, the excess cytokines (IL-17, IL-21, IL-22, etc.) act on intestinal epithelial cells, macrophages, and colon myofibroblasts, induce proinflammatory chemokines and other proinflammatory mediators, mediate the early mobilization of granulocytes, and participate in the early inflammatory mediator response, significantly greater than the immune protective effect of cytokines secreted by Treg cells (TGF-β, IL-10, etc.); the body is prone to induce IBD. In this paper, the TCM monomer, extract, and compound (such as Abelmoschus manihot, Daphnetin, epigallocatechin-3-gallate, Baitouweng Decoction, and compound sophorae decoction) are exactly the different stages of the differentiation and regulation of Th17 cells and Treg cells, thus inhibiting the differentiation and production of Th17 cells, reducing the number of associated damage factors that it has secreted, reducing the inhibition of Treg cells differentiation and promoting its production, increasing the number of associated protective factors it secreted, further resulting in restoration of the intestinal immune balance, achieving therapeutic purposes.Abbreviations. AhR: aryl hydrocarbon receptor; AMPK: adenosine 5′-monophosphate- (AMP-) activated protein kinase; ACC1: acetyl-CoA carboxylase 1; CYP1A1: cytochromeP4501A1; CREB: cAMP-response element binding protein; DC: dendritic cells; DNMT-1: DNA methyltransferase-1; Foxp3: forkhead-like protein 3; GPR41: G-protein receptor 41; HIF-1α: hypoxia-inducible factor 1-alpha; IL: interleukin; miR-302: microRNA-302; MAPK: mitogen-activated protein kinase; NF-κB: nuclear factor kappa-B; PPARγ: peroxisome proliferator-activated receptor γ; PHD2: prolyl hydroxylase 2; RORγt: receptor-associated orphan receptor γt; RORC: receptor-associated orphan receptor; STAT3: transcription protein 3; STAT3: transcription protein 3; TGF: transforming growth factor; TLR4: toll-like receptor 4.