Determining important mechanisms that contribute to IBD
Research type
Research Study
Full title
Determining important mechanisms that contribute to inflammatory bowel disease.
IRAS ID
163276
Contact name
Mark Travis
Contact email
Sponsor organisation
University of Manchester
Duration of Study in the UK
5 years, 0 months, 1 days
Research summary
Our immune system is crucial in keeping us healthy by protecting us from infection. However, the immune system must be carefully controlled so that it only attacks harmful pathogens, and not the organs and tissues of our own body. If the immune system starts to attack our own body, so-called autoimmune diseases can occur. A highly prevalent autoimmune disease in Western societies is inflammatory bowel disease (IBD), and affects hundreds of thousands of people in the UK. IBD occurs when the body’s immune system attacks our gut, often resulting in severe pain and weight loss. Despite the devastating effects of IBD, current treatments are poor and little is known about the underlying causes of IBD. Thus, gaining a better understanding how IBD develops will provide important potential new targets to treat the conditions.
Our study, arising from a recently awarded Medical Research Council-funded project grant, aims to discover important molecular and cellular pathways that contribute to the development and symptoms of IBD. Specifically, we will identify focus on identifying genes, cells and molecules that are altered in IBD patients versus healthy individuals, with a focus on cells of the adaptive immune system (T-cells, regulatory T-cells, dendritic cells). To achieve these aims, we will obtain intestinal samples from patients undergoing scheduled endoscopy or surgery and compare 'healthy' tissue to inflamed tissue from IBD patients. Our work will therefore aim to uncover important biological differences that contribute to IBD, therefore identifying potential therapeutic targets for this devastating disease.REC name
North West - Greater Manchester South Research Ethics Committee
REC reference
15/NW/0007
Date of REC Opinion
18 Feb 2015
REC opinion
Further Information Favourable Opinion