An immune defect that may set Crohn's disease in motion
Crohn's disease, a condition characterized by widespread inflammation in the gut, may arise from a weakened immune response, according to new research from the University of Toronto's Temerty Faculty of Medicine.
A new study from the University of Toronto's Temerty Faculty of Medicine suggests that Crohn's disease may be triggered by a weakened immune response, rather than inflammation as previously thought. Researchers led by Dana Philpott, a professor of immunology, analyzed the activity of T cells during viral infection in animal models with and without a functional NOD2 gene.
They discovered that fewer T cells were recruited to gut lymph nodes in the absence of NOD2, and these cells were less effective at fighting off subsequent infections. The study, published in Nature Immunology, challenges existing theories about the origins of Crohn's disease, a type of inflammatory bowel disease. Philpott and his team believe they have uncovered a mechanism that could explain the disease's onset before the onset of inflammation.
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