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Study Reveals Clues About the Genetic Control of Immune Cells

Published 11 September 2020

Dr James Lee's work looks at how immune cells involved in the development of Crohn's and Colitis are controlled. Using a ground-breaking technique, his team have shed some light on how small differences in our DNA can cause disease-associated immune changes.

More than 200 genetic variations can affect your risk of developing Crohn's or Colitis. However, scientists have been unable to figure out what these variations do, or why they contribute to someone developing Crohn's or Colitis. This type of research is very technically difficult, and until recently researchers could only study one genetic variation at a time, making progress very slow.

James and his team have overcome this by using a new technique to simultaneously test the effect of many genetic variations directly in immune cells. This gave them a really powerful tool to test their ideas about what causes the damaging inflammation seen in Crohn's and Colitis. Importantly, in their recent publication back in April they describe how one particular genetic variation leads to uncontrolled inflammation, which explains why this genetic variation predisposes people to immune-mediated diseases like Crohn's and Colitis.

The success of genetic studies in Crohn’s and Colitis has provided an incredible opportunity to better understand these diseases, but the complexity of figuring out how genetic variations predispose to disease had been a major obstacle for everyone in the field. We were delighted to have found a way to overcome this and can now use this approach to gain new insights into disease biology. This work could not have been done without the generous funding from Crohn’s and Colitis UK.


Dr James Lee
Lead author of the study, University of Cambridge

This work has opened the door to better understanding of the biology underlying inflammatory bowel diseases (IBD). The team hope that this will help identify new therapeutic targets and, in turn, speed up the development of better treatments. Indeed, James and his team have developed partnerships with pharmaceutical companies to take this idea one step closer to patients.

James and his team successfully show that the intelligent application of new techniques can reveal so much about disease biology.

Using this genetic technique to identify causes of inflammation in Crohn's and Colitis is particularly exciting because new drug targets that have been developed from genetic analyses are much more successful in clinical trials than those that weren't. We hope that by funding James' work we have helped open the door to new therapeutic opportunities for these conditions.


Dr Jane Fraser
Research Programme Officer, Crohn's & Colitis UK

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