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A team of scientists has discovered mechanisms of abnormal immune cell function that may lead to Crohn’s disease, an inflammatory bowel disease (IBD).
Crohn’s disease causes chronic inflammation of the gastrointestinal (GI) tract, and symptoms can include abdominal pain, diarrhoea, weight loss, anaemia, and fatigue.
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White blood cells in the GI tract known as intraepithelial lymphocytes express the gamma delta T cell receptor (gamma delta IELs), which prevent infection and provide surveillance for the intestinal barrier. These gamma delta IELs are often reduced in patients with active Crohn’s disease.
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A research team led by Mount Sinai said their study is the first to show that gamma delta IELs are critical to maintain a balance between pro-inflammatory and regulatory immune responses, and these cells are impaired during the onset and progression of long-term inflammation in the lower small intestine.
“Previous studies assessing patient biopsies revealed a decrease in gamma delta IELs in those with active IBD. However, it was unknown whether the loss of these cells was a cause or consequence of disease,” said Karen Edelblum, Associate Professor of Pathology, Molecular and Cell-Based Medicine at the Icahn School of Medicine at Mount Sinai.
The findings, published in Science Immunology, now show that gamma delta IELs are substantially decreased weeks before clinical or histological evidence of disease in a mouse model of Crohn’s disease-like ileitis.
Furthermore, “we were able to generate a timeline of events leading to the dysregulation of gamma delta IELs that mirrored findings from prior studies in patients with IBD,” Edelblum said.
The researchers said loss of gamma delta IELs could be used as a predictive biomarker for disease relapse or patient responsiveness to treatment.
Additionally, development of future therapies that boost the function of gamma delta IELs may provide a new way to maintain remission in IBD patients or prevent disease development in susceptible individuals.
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