Inflammatory bowel disease pathogenesis mediated by Th17 cells: cytokines, microbiota, and therapies

• Published in: Journal of Biomedical and Translational Research Vol. 25; no. 2; pp. 158 - 32
• Main Authors: Ji-Hyun Park, Min Hyeok Lee, Chan-Su Park
• Format: Journal Article
• Language: English
• Published: 충북대학교 동물의학연구소 30.06.2024
• Subjects: microbiota; ulcerative; colitis; inflammatory bowel diseases; cytokines; Th17 cells
• ISSN: 2508-1357; 2508-139X

Inflammatory bowel disease (IBD) is a chronic condition characterized by continuous inflammation of the gastrointestinal tract that varies in intensity over time. IBD is caused by several factors including aberrant gut flora, immunological dysregulation, altered environmental conditions, and genetic variations. However, the pathogenesis of IBD remains unclear. Studies have indicated that an imbalance between T helper 17 (Th17) and regulatory T (Treg) cells contributes significantly to the development of IBD. Intestinal Tregs suppress inflammation and are critical for maintaining tissue homeostasis. Th17 cells are known to play an important role in the development and pathogenesis of IBD and provide non-inflammatory support for the integrity of the intestinal barrier against bacterial and fungal infections. Therefore, the Th17/Treg cell balance is crucial in the pathogenesis of IBD and gut integrity. The microenvironment of the intestinal mucosal immunity is regulated by the secretion of cytokines associated with Th17 cells and Tregs. Several studies have indicated that the gut bacteria contribute to the control of the immune milieu and play a key role in the regulation of Th17 cell development. Intestinal bacteria and cytokines control Th17 cell development. Th17 cells secrete cytokines that regulate the immune microenvironment in the gut mucosa. This review provides an overview of Th17 cells and examines the strategies for treating patients with IBD using Th17 cell-targeted drugs.