Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is a chronic relapsing intestinal inflammation with increasing global incidence. It results from an aberrant immune response to gut microbes, influenced by genetic, environmental, and microbial factors. Recent research highlights the role of genetic susceptibility, environmental factors, microbial flora, and immune responses in IBD pathogenesis. Genetic studies have identified 163 susceptibility gene loci, with overlaps between CD and UC suggesting shared genetic predispositions. However, genetic factors alone do not fully explain IBD, indicating interactions with environmental and microbial elements. The innate immune response, particularly through NOD2, plays a crucial role in IBD, alongside adaptive immunity involving Th17 cells and IL-23/IL-17 pathways. Environmental factors such as smoking, diet, and air pollution also contribute to IBD risk. Microbial factors, including altered gut microbiota and adherent invasive E. coli, are implicated in disease development. The interplay between genetic, environmental, and microbial factors, along with immune responses, is central to IBD pathogenesis. Future research aims to clarify these interactions to better understand and treat IBD.Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is a chronic relapsing intestinal inflammation with increasing global incidence. It results from an aberrant immune response to gut microbes, influenced by genetic, environmental, and microbial factors. Recent research highlights the role of genetic susceptibility, environmental factors, microbial flora, and immune responses in IBD pathogenesis. Genetic studies have identified 163 susceptibility gene loci, with overlaps between CD and UC suggesting shared genetic predispositions. However, genetic factors alone do not fully explain IBD, indicating interactions with environmental and microbial elements. The innate immune response, particularly through NOD2, plays a crucial role in IBD, alongside adaptive immunity involving Th17 cells and IL-23/IL-17 pathways. Environmental factors such as smoking, diet, and air pollution also contribute to IBD risk. Microbial factors, including altered gut microbiota and adherent invasive E. coli, are implicated in disease development. The interplay between genetic, environmental, and microbial factors, along with immune responses, is central to IBD pathogenesis. Future research aims to clarify these interactions to better understand and treat IBD.