The article explores the role of interleukin 1β (IL-1β) in the pathogenesis of inflammatory bowel disease (IBD). IL-1β is a significant mediator of inflammation and tissue damage in IBD, and its balance with its endogenous inhibitor, IL-1Ra, plays a critical role in both the initiation and regulation of inflammation. The review summarizes the molecular and cellular characteristics of IL-1β, its role as a modulator of intestinal homeostasis and an activator of inflammatory responses, and the involvement of microRNAs in regulating IL-1β-related inflammatory responses in IBD. IL-1β is involved in several aspects of IBD, including the induction of pro-inflammatory responses through immune cell recruitment and activation, intestinal barrier disruption, and the modulation of T helper (Th) cell differentiation, particularly Th17 cells. Dysbiosis in the gut can also stimulate immune cells to release IL-1β, promoting inflammation. Additionally, microRNAs play a central role in IL-1β-related signaling during IBD, particularly in maintaining intestinal epithelial homeostasis. The article concludes that targeting IL-1β or its receptors represents a promising therapeutic approach, and further research into post-transcriptional modifications of IL-1β may elucidate its complex role in immunomodulation.The article explores the role of interleukin 1β (IL-1β) in the pathogenesis of inflammatory bowel disease (IBD). IL-1β is a significant mediator of inflammation and tissue damage in IBD, and its balance with its endogenous inhibitor, IL-1Ra, plays a critical role in both the initiation and regulation of inflammation. The review summarizes the molecular and cellular characteristics of IL-1β, its role as a modulator of intestinal homeostasis and an activator of inflammatory responses, and the involvement of microRNAs in regulating IL-1β-related inflammatory responses in IBD. IL-1β is involved in several aspects of IBD, including the induction of pro-inflammatory responses through immune cell recruitment and activation, intestinal barrier disruption, and the modulation of T helper (Th) cell differentiation, particularly Th17 cells. Dysbiosis in the gut can also stimulate immune cells to release IL-1β, promoting inflammation. Additionally, microRNAs play a central role in IL-1β-related signaling during IBD, particularly in maintaining intestinal epithelial homeostasis. The article concludes that targeting IL-1β or its receptors represents a promising therapeutic approach, and further research into post-transcriptional modifications of IL-1β may elucidate its complex role in immunomodulation.