For the first time, a major trigger in inflammatory bowel disease (IBD) and related conditions has been identified, and existing drugs can stamp it out, in what scientists call a "massive step" in successfully treating these debilitating chronic conditions. Researchers at the Francis Crick Institute, in collaboration with University College London (UCL) and Imperial College London (ICL), have uncovered a problem gene enhancer that stimulates action along a specific biological pathway that causes IBD inflammation. Until now, our incomplete knowledge of what drives IBD has made it incredibly hard to find a 'one-size-fits-all' medical intervention.
This enhancer was found in an area of DNA known as a 'gene desert' – where genetic material doesn't code for proteins – which has already been linked to IBD and other autoimmune conditions. While the enhancer, a section of DNA, doesn't code for proteins, it directly influences the protein production of nearby genes. What's more, they found that this enhancer was only active in immune cells known as macrophages – a key immune cell in IBD – and it boosted the gene .
Higher activity reflected higher risk of inflammation. "Using genetics as a starting point, we've uncovered a pathway that appears to play a major role in IBD and other inflammatory diseases," said James Lee, group leader of the Genetic Mechanisms of Disease Laboratory at the Crick. Zooming in on , the scientists discovered that it was driving inflammation from macro.
