Inflammatory bowel diseases (IBD), which include Crohn's disease and ulcerative colitis, may not be two forms of one disease, but rather a whole group of different diseases with different mechanisms of development. This conclusion was reached by scientists from the University of Oxford, Newcastle University, and the University of Cambridge.
IBD represents chronic diseases characterized by prolonged inflammation of the gastrointestinal tract mucosa. In ulcerative colitis, inflammation affects the large intestine, while in Crohn's disease, it can affect any part of the gastrointestinal tract. Typically, these conditions develop in adolescence or early adulthood and accompany a person throughout their life.
Despite years of research, the exact causes of IBD remain unclear. It is believed that genetic predisposition and immune system dysfunction play an important role.
The results of a new study published in the New England Journal of Medicine have made an important step towards understanding the nature of these diseases. Researchers analyzed data from 4,909 patients with IBD and identified a previously unknown mechanism of disease development in some patients.
The first significant discovery was the detection of autoantibodies to interleukin-10 (IL-10), one of the key anti-inflammatory molecules of the immune system. Such autoantibodies were found in approximately 3.5% of patients with both Crohn's disease and ulcerative colitis. They were completely absent in healthy individuals.
Interleukin-10 acts as a kind of "brake" for the immune system, limiting inflammatory processes. When autoantibodies block the action of IL-10, this protective mechanism ceases to function, and inflammation becomes uncontrolled.
The second discovery is related to genetics. All patients with detected autoantibodies to IL-10 were found to carry the genetic variant HLA-DRB1*01:03. This genetic factor has long been considered one of the most significant risk factors for the development of inflammatory bowel diseases.
The link between the HLA-DRB1*01:03 variant and severe forms of IBD was discovered about 30 years ago, but the mechanism of this influence remained a mystery. The new study showed that this genetic variant increases the likelihood of developing an autoimmune reaction against IL-10.
According to the researchers, the obtained data opens up prospects for the creation of new diagnostic and treatment methods. In the future, there may be special blood tests that allow for the identification of patients with this type of disease, as well as drugs that directly target the autoantibodies or the cells that produce them.
Scientists believe that this discovery could be an important step towards personalized treatment of inflammatory bowel diseases.
