Health
Mount Sinai-led research reveals the mechanisms behind inflammation in Crohn's disease
A research team led by Sinai Mountain reveals the mechanisms of abnormal immune cell function that can lead to Crohn's disease. Scientific Immunology Researchers said their findings could better understand the development of the disease and inform the development and design of new therapies to prevent inflammation before they begin with chronic disorders.
Crohn's disease is chronic inflammatory bowel disease (IBD) inflammation It may include those in the gastrointestinal (GI) area and symptoms abdominal paindiarrhea, weight loss, anemia, fatigue. Inflammation is the body's natural response to infection or injury, but long-term untreated inflammation can cause damage to healthy cells, tissues and organs. GI leukocytes, known as intraepithelial lymphocytes, express the gamma delta T cell receptor (gamma delta IELS), which prevents infection and provides monitoring of the intestinal barrier. These gamma deltailes are often reduced in patients with active Crohn's disease.
The researchers said their research was the first to show that gamma delta IELS is important to maintain a balance between proinflammatory and regulatory immune responses, and that these cells are impaired during the onset and progression of low intestinal long-term inflammation.
Previous studies assessing patient biopsies revealed a reduction in gamma delta IELS in patients with active IBD. However, it was unclear whether the loss of these cells was the cause or consequence of the disease. Currently, our findings show that gamma deltailes are significantly reduced several weeks before evidence of clinical or histological disease in mouse models of enteritis, such as clone disease. Furthermore, we were able to generate a timeline of events leading to dysregulation of gamma deltaile, reflecting findings from previous studies in patients with IBD. ”
Karen Edelblum, PhD, Corresponding authors, Associate Professor of Pathology, Molecular and Cell-Based Medicine, ICAHN School of Medicine, Mt. Sinai
The researchers analyzed human disease using a mouse model of Crohn's disease-like inflammation in the lower small intestine. Before tissue damage began, they found that proinflammatory proteins impair communication between gamma deltaile and adjacent intestinal epithelial cells. As a result, most of these gamma deltailes were unable to survive, significantly impairing barrier monitoring. The researchers also identified that gamma delta IELS lost the ability to suppress other proinflammatory IELS that cause tissue damage, indicating that early loss of regulated gamma delta IELS may contribute to the activation of inflammation in Crohn's disease.
Researchers said that loss of gamma deltaile can be used as a prediction Biomarkers Patient's response to disease recurrence or treatment. Furthermore, the development of future therapies that enhance the function of gamma delta IELS may provide new ways to maintain remission in IBD patients and to prevent the onset of disease in susceptible individuals.
Researchers from Rutgers University, Case Western Reserve University and Children's Hospital of Los Angeles contributed to this study. This study was supported by grants from the National Institutes of Health, the Clones and Colinitis Foundation, *Stars, and the New Jersey Cancer Research Committee.
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Journal Reference:
Xu, W. , et al. (2025). Intraepithelial lymphocyte dysfunction precedes Crohn's disease-like disorder. Scientific Immunology. doi.org/10.1126/sciimmunol.adk7429.
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