Appendix in ulcerative colitis pathogenesis and therapy: An updated narrative review

Figure 1 Mechanisms of appendix-mediated ulcerative colitis pathogenesis. Appendiceal inflammation may initiate or exacerbate ulcerative colitis (UC) pathogenesis through multiple interconnected mechanisms, including dysregulation of T and B lymphocytes, impaired immune tolerance, and altered cytokine signaling. In addition, disruption of the appendiceal microbiota may promote gut dysbiosis and facilitate the persistence of pathogenic bacteria. Defective bulk autophagy and xenophagy in the appendix may represent mechanisms contributing to UC pathogenesis and warrant future exploration. GALT: Gut-associated lymphoid tissue; Th: T helper cell; Treg: Regulatory T cell; IBD: Inflammatory bowel disease; IL: Interleukin.