Inflammatory bowel disease is a general name used for two diseases that involve the ongoing inflammation of a person’s gastrointestinal tract, namely Crohn’s disease and ulcerative colitis. Both forms of IBD can result in diarrhoea, pain in the abdomen, bloody stools, tiredness, and weight loss. This condition happens when the immune system overreacts, causing inflammation.

Exactly what causes this overreaction, though, was unclear until now. A new study, published in the journal Science Immunology, lays the groundwork for a better understanding of how and why ulcerative colitis occurs and possible future therapies to treat the disease.

The research identified the presence of a dysfunctional immune cell that continues to overreact for a long time.

The research
A team of scientists from across the world conducted this experiment by analyzing the immune cells present in rectal biopsies or blood of people with IBD. They found it easier to study ulcerative colitis, as, unlike Crohn’s disease, it affects the same part of the gut in everyone who has it.

They used mRNA sequencing and antigen receptor sequencing on rectum samples of seven people with the condition and nine of those without.

The findings
Memory T cells determine the specific kind of immune response of the body, in case the pathogen or infection return.

The researchers found high levels of a certain subtype of a kind of T cell (called CD8+) in people with ulcerative colitis. The subtype, known as TRM, was in a hyper-excitable state. It was seen that these cells readily reproduce and give rise to a significant number of cytokines that damage the person’s gastrointestinal tissue.

Further, the researchers found that this T cell subtype could also escape into a person’s bloodstream, which provides an explanation as to how IBD affects not just the intestines but other parts of the body as well.

While management of IBD has improved, some people still do not respond well over the long term. The researchers’ work opens the door to possible future treatments. However, the next step is to see if it may be possible to target and eliminate this T cell subtype directly.

References

  1. Brigid S. Boland, Zhaoren He, Matthew S. Tsai, Jocelyn G. Olvera, Kyla D. Omilusik, Han G. Duong, Eleanor S. Kim, Abigail E. Limary, Wenhao Jin, J. Justin Milner, Bingfei Yu, Shefali A. Patel, Tiani L. Louis, Nadia S. Kurd, Alexandra Bortnick, Lauren K. Q
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