Defining the therapeutic potential of CD25 (IL2-R) blockade as a novel treatment for genetically stratified Crohn’s disease patients
Professor Graham Lord
Institution or company
King's College London
Inflammatory bowel disease (IBD) can cause disabling symptoms, impaired quality of life, and serious complications. Many patients will be hospitalised during the course of their treatment, and some will need to undergo major surgery.
At present, even the best treatments fail to keep the disease under control for a third of patients. Developing new treatments is, therefore, vitally important.
IBD is thought to be caused by inappropriate activation of the intestinal immune system, triggering long-lasting inflammation of the gut. Certain immune cells plan an instrumental role in initiating and continuing this damaging inflammatory process.
This research focuses on types of cell known as effector (Teffs) and regulatory T cells (Tregs), which have an important role in the gut of IBD patients. Tregs suppress immune responses in the intestine, and over-active Teffs can cause inflammation. Therefore, the balance between Tregs and Teffs in the intestine is key.
Our group of researchers have recently discovered that a genetic variation controls the balance between Teffs and Tregs by changing the amount of a receptor which cells show on their surface. Importantly, there are medicines already in use in other conditions which act to block this receptor, which we believe could be used to treat patients with IBD who carry this genetic variation.
This project aims to test the theory that blocking this receptor could be an effective treatment for Crohn’s disease in the laboratory environment, and we believe that this will lead to clinical trials in patients who carry the genetic variation.
We also believe that this work will be an important step towards the goal of ‘personalised medicine’, whereby individual treatments are tailored to patients most likely to benefit from them, and least likely to suffer unwanted side-effects.