Researchers Uncover Possible Triggers of Inflammatory Bowel Disease

New York: A new study has shed light on the underlying immune mechanisms that may drive Crohn’s disease, a common form of inflammatory bowel disease (IBD). Researchers from Mount Sinai have identified dysfunction in a specific group of immune cells, known as gamma delta intraepithelial lymphocytes (gamma delta IELs), which appears to play a critical role in triggering and sustaining chronic intestinal inflammation.

Crohn’s disease is a debilitating condition characterized by persistent inflammation of the gastrointestinal (GI) tract. Patients often experience symptoms such as abdominal pain, diarrhoea, weight loss, fatigue, and anaemia. Although previous studies have observed a reduction in gamma delta IELs in individuals with active IBD, it remained unclear whether the loss of these cells was a result of the disease or a contributing factor.

In the latest research, published in Science Immunology, scientists demonstrated for the first time that these immune cells are crucial for maintaining balance between pro-inflammatory and regulatory immune responses within the gut. The team used a mouse model of Crohn’s disease-like ileitis to track the progression of inflammation. Their findings revealed a significant decline in gamma delta IELs several weeks before any clinical or histological signs of disease appeared.

Lead researcher Karen Edelblum, Associate Professor at the Icahn School of Medicine at Mount Sinai, explained that the early loss of gamma delta IELs disrupts intestinal immune regulation, potentially setting the stage for long-term inflammation in the lower small intestine. This decline mirrors patterns previously observed in human biopsy studies, strengthening the link between these immune cells and IBD pathogenesis.

The research opens new possibilities for predicting disease onset or relapse. According to the team, monitoring gamma delta IEL levels could serve as a valuable biomarker to assess patient risk or treatment response. Furthermore, they suggest that therapies aimed at enhancing the function of these immune cells may offer a novel strategy to maintain remission or prevent Crohn’s disease in individuals at risk.

These findings represent a significant step forward in understanding Crohn’s disease and may pave the way for targeted therapies to improve patient outcomes.