T cells are immune cells that drive the development of inflammatory bowel disease (ulcerative colitis and Crohn’s disease) through the way that they react to the bacteria that are resident in our gut.

Until recently it was thought that T cells continuously enter and leave the gut via the bloodstream but a new type of T cell has been found that resides in the gut for extended periods of time. This type of T cell is known as a resident memory T cell or Trm.

This PhD study, funded by the Masonic Charitable Foundation has three aims:

  • To identify and characterise Trm in the gut of patients with IBD and a healthy control group;
  • to determine the contribution to inflammation of Trm in patients with IBD; and
  • to relate Trm function to outcomes following therapy.

The researchers

The research will be led by Professor James Lindsay and Dr Andrew Stagg at Queen Mary University of London. The work will be undertaken day-to-day by a PhD student.

Why analyse the role of T cells in inflammatory bowel disease?

Inflammatory bowel disease (IBD; Crohn’s disease and ulcerative colitis) is a life-long, debilitating and sometimes life-threatening condition. It is caused through an uncontrolled immune response to aspects of the bacteria that reside within the gut.

Genes play a role in making an individual susceptible to the condition as does the environment (diet, exercise, pollution, infection etc.) but this is currently poorly understood.

There are around 300,000 IBD patients in the UK and 1 in 20 of these suffer from a severe form of the disease that dominates their life. Most people will be first diagnosed in adolescence.

IBD is expensive to treat and the average life time cost of treating an IBD patient is comparable to that of a patient with coronary heart disease or cancer, costing the NHS over £500 million each year. There is no cure for IBD and control of inflammation with drugs or surgical removal of affected tissue are often not satisfactory over the long-term.

Biological therapies targeting immune responses have had major impact on treatment and approximately 30,000 UK patients are currently receiving a biologic which now account for 75% of healthcare costs. However, up to one third of patients do not respond and a similar proportion lose response over time. The failure of some therapies for particular patients is likely to be related to differences in the how their individual immune responses react (immune pathways).

This work will help us to further our understanding of the immune pathways that drive intestinal inflammation and how these vary between individual patients with either Crohn’s disease or Ulcerative Colitis. Our aim is therefore to increase personalisation in therapies for individuals with IBD and to bring down the costs to the NHS of treating the lifelong effects of the condition.

We are very grateful to the Masonic Charitable Foundation which is funding this study over three years.