Editorial on the Research TopicThe mechanism of immune cells in the development of inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC)Inflammatory bowel disease (IBD), which includes Crohn's disease (CD) and ulcerative colitis (UC), is characterized by intermittent chronic inflammation of the gastrointestinal tract, due to a dysregulated immune response against intestinal mucosa, leading to bowel damage (1, Russo et al.). In IBD, the sealed intercellular junctions are damaged, either from a primary barrier function defect or from severe inflammation. Excessive inflammatory response leads to continued deterioration of the epithelium and exposure to the intestinal microbiome (bacteria, fungi, viruses, and their genes living in the gut), thereby further worsening the inflammation (2, 3).Colitis-associated colorectal cancer (CAC) is the most critical IBD complication (Rubin et al.). The carcinogenesis in IBD is a multistep progression, due to increasing degrees of histologic, molecular, and endoscopic alteration, from no dysplasia against chronic inflammation to low-grade dysplasia to high-grade dysplasia and eventually neoplasia (4).In addition, inflammation and cancer are closely related, as it has been welldocumented (5, 6). It induces genetic and epigenetic alterations transmissible to epithelial cell progeny (7), promoting epithelial turnover. Finally, inflammationFrontiers in Immunology frontiersin.org 01