Scientists Uncover Mechanisms Leading to Inflammatory Bowel Disease

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Scientists Uncover Mechanisms Leading to Inflammatory Bowel Disease

Synopsis

Researchers have identified mechanisms linked to abnormal immune cell function that may contribute to Crohn’s disease, a form of inflammatory bowel disease (IBD). Their findings reveal critical insights into the role of gamma delta IELs in maintaining immune balance.

Key Takeaways

  • Discovery of immune cell mechanisms related to Crohn's disease.
  • Gamma delta IELs play a vital role in immune response balance.
  • Decrease in gamma delta IELs may indicate disease onset.
  • Potential for predictive biomarkers in treatment responses.
  • Future therapies could target gamma delta IEL function.

New York, March 23 (NationPress) A group of researchers has identified mechanisms related to abnormal immune cell behavior that could contribute to Crohn’s disease, a type of inflammatory bowel disease (IBD).

Crohn’s disease leads to chronic inflammation in the gastrointestinal (GI) tract, with symptoms including abdominal pain, diarrhea, weight loss, anemia, and fatigue.

Intraepithelial lymphocytes, which are white blood cells in the GI tract, express the gamma delta T cell receptor (gamma delta IELs). These cells are crucial for preventing infections and monitoring the intestinal barrier. However, gamma delta IELs are often diminished in individuals suffering from active Crohn’s disease.

A research team from Mount Sinai highlighted that their investigation is the first to demonstrate the importance of gamma delta IELs in balancing pro-inflammatory and regulatory immune responses, noting that these cells become dysfunctional during the onset and progression of chronic inflammation in the lower small intestine.

“Prior studies analyzing patient biopsies indicated a reduction in gamma delta IELs among those with active IBD. Yet, it was unclear whether the depletion of these cells was a cause or a consequence of the disease,” stated Karen Edelblum, Associate Professor of Pathology, Molecular and Cell-Based Medicine at the Icahn School of Medicine at Mount Sinai.

The study's results, published in Science Immunology, reveal that gamma delta IELs significantly decrease weeks before any clinical or histological signs of disease appear in a mouse model that simulates Crohn’s disease-like ileitis.

Additionally, “we successfully established a timeline that outlines the events leading to gamma delta IEL dysregulation, which aligns with previous findings in patients with IBD,” said Edelblum.

The research team noted that the loss of gamma delta IELs could serve as a predictive biomarker for disease recurrence or treatment responsiveness.

Moreover, the development of future therapies aimed at enhancing the functionality of gamma delta IELs may offer new strategies to sustain remission in IBD patients or prevent the onset of the disease in individuals at risk.