Inflammatory bowel disease (IBD) is a chronic autoimmune disorder that affects the gastrointestinal tract. It includes two primary forms of inflammatory bowel disease - Crohn's disease (CD) and ulcerative colitis (UC) - that share some common clinical features such as abdominal pain, diarrhea, and rectal bleeding. Although the precise etiology of IBD remains unclear, it is believed that genetic, environmental, and immunological factors play a role in the development of this condition. Recent studies have suggested that epigenetic modifications in immune cells may contribute to the pathogenesis of IBD. This article will discuss the role of immunoepigenetic regulation in the development of IBD. Epigenetic modifications are heritable changes in gene expression that do not involve alterations to the DNA sequence. Epigenetic mechanisms include DNA methylation, histone modifications, and non-coding RNA expression, all of which play important roles in the regulation of gene expression. Dysregulation of epigenetic mechanisms can lead to aberrant gene expression and contribute to the development of diseases such as cancer, autoimmune disorders, and neurodegenerative diseases. In the context of IBD, recent studies have highlighted the importance of epigenetic modifications in immune cells.
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