A new study has revealed an abnormal immune response that may be responsible for inflammatory bowel disease in a subset of patients.
inflammation of the digestive tract. The disease includes two main types: Crohn's disease, which can affect any part of the digestive system, and ulcerative colitis, which is limited to the colon and rectum.
Although patients may experience similar symptoms, the underlying causes of inflammation can vary from person to person, prompting researchers to search for more specific pathological mechanisms that can be targeted therapeutically.
In the new study, published in the New England Journal of Medicine, researchers found that about 3.5% of patients with inflammatory bowel disease carry autoantibodies that attack an important anti-inflammatory protein known as interleukin-10 (IL-10).
This protein plays a crucial role in suppressing the inflammatory response within the body. When autoantibodies disrupt its function, the body's ability to control inflammation is impaired, which can contribute to disease progression.
The researchers analyzed blood samples from over 4,900 patients with inflammatory bowel disease, as well as over 1,000 individuals without the disease. The results showed the presence of these antibodies in 173 patients, while they were almost entirely absent in the control group.
Laboratory experiments have also shown that exposing immune cells to blood samples from patients carrying these antibodies leads to a decrease in "interleukin-10" levels and stimulates a clear inflammatory response.
Researchers believe that genetics may play a significant role in this process. The study showed that carriers of the HLA-DRB1*01:03 gene variant are significantly more likely to develop autoantibodies that disrupt the function of interleukin-10 compared to others.
This genetic variant is one of the most prominent genetic risk factors associated with ulcerative colitis, and has previously been linked to more severe cases of inflammatory bowel disease, which may require surgical intervention.
Dr. Holm Oleg, a pediatric gastroenterologist at Oxford University, said that identifying the factors that lead to the formation of these autoantibodies is an important step towards better understanding the disease, noting that the 3.5% figure represents a significant number of patients worldwide.
Dr. Brad Pasternak, medical director of the Inflammatory Bowel Disease Clinic at Children's Hospital Phoenix, explained that most current treatments target inflammation in general, but their effectiveness varies from patient to patient. He added that the study's findings could pave the way for the development of targeted therapies that address the underlying cause in each patient group.
Researchers believe that the importance of the results is not limited to developing treatments, but extends to improving early diagnosis, as genetic tests may help in the future to identify patients most prone to developing these autoantibodies, allowing for faster and more accurate therapeutic intervention.
